Daniel Drucker, Ozempic's father: "If funding was provided for everyone who wants to lose weight, there wouldn't be any money left for anything else."

Daniel Drucker (Montreal, 68) speaks a little Spanish at the BBVA Foundation headquarters in Bilbao, where he's about to begin a long round of interviews worthy of a Nobel Prize winner. He's in the Basque city to receive the Frontiers of Knowledge Prize and says he only knows the important words in this language. "A wine, a beer, a snack," jokes this Canadian endocrinologist, son of Holocaust survivors and one of the few people who can truly say they've changed the world.

Drucker, now a professor at the University of Toronto and a researcher at Mount Sinai Hospital in that city, receives the award "for the discovery and characterization of the biologically active form of the hormone glucagon-like peptide-1 (GLP-1). The reason sounds esoteric, and the complex science behind it is, but the products of his knowledge are popular culture. The famous Ozempic , a diabetes drug that rose to fame when a mysterious wave of thinness swept through Hollywood in 2022, has made the company that produces it, the Danish Novo Nordisk, the most valuable in Europe, and the product a hope for the millions hungry for aesthetics.

Question: What do you think about the hype surrounding weight-loss drugs that arose from your research?

Answer: Sometimes it's excessive. When I go out, if I go to a store, to a soccer game, if I turn on the television, all I see is Ozempic, everywhere. It's really present in popular culture, and sometimes it's excessive, no doubt. But I also think it's an opportunity to show the importance of science and being able to help people living with obesity who previously didn't have good treatments. Journalists call me several times a day, and it's a privilege to receive so much attention, but sometimes it's too much.

Q. It's a great triumph for science, but at the same time, the fact that these obesity drugs are so successful tells us that there is a serious social problem .

A: Yes. I think we don't fully understand the obesity epidemic. When I was young, we were told that the world's biggest problem was hunger. And today, perhaps, that has been replaced in many parts of the world by obesity. And genetics haven't changed, so we have to ask ourselves: what has changed in the environment, in society, in food, in the chemicals that surround us?

We don't know exactly what's contributing to the obesity epidemic. It's very easy to say "ultra-processed foods," "McDonald's," "the food industry"—and all of those probably contribute to the problem. But I think that, at the same time that we have very good science developing drugs, we also need equally strong science to help us understand why we have this obesity epidemic. The ideal would be to prevent obesity from developing, not just treat it.

When I go out, if I turn on the TV, I see Ozempic everywhere. Sometimes he has too much hype.

Q. One aspect of your research is that it has shown that people who are obese or overweight don't have a willpower problem, but rather that their bodies don't produce the necessary signals to stop their appetite. From a scientific perspective, does it make sense that, as is the case in Spain, these drugs are funded for people with diabetes, but not for treating obesity?

A. For many years, there was a lot of debate about this. Some people said, "Why should we approve weight-loss drugs? Maybe they just make people look better, buy new clothes, or feel a little better... But that doesn't actually improve their health."

But two and a half years ago, we had a very important study, the SELECT trial . It included people without type 2 diabetes, but who were overweight or obese and had a history of heart disease. They were treated with semaglutide [the active ingredient in Ozempic] for three and a half years. And what did we see? A 20% reduction in heart attacks, strokes, and deaths, and a 19% reduction in total deaths in just three and a half years.

This study has been very important in reminding people that obesity is a serious disease, especially in people with cardiovascular disease. As we gather more evidence about the benefits of these drugs beyond weight loss—such as reducing kidney disease, heart attacks, strokes, and so on—it will be easier to justify funding them.

But we have to understand that governments and insurers are afraid of the cost. If everyone who wants to lose weight were funded with GLP-1, there wouldn't be any money left for anything else. We only have a certain budget for healthcare and medicines, and we try to allocate it where it achieves the greatest benefit. And I think we'll see increasing evidence that obesity with comorbidities—people with heart, liver, or kidney disease—conveys a serious risk of developing very costly pathologies. We're starting to generate the data that will allow us to talk to governments and insurers again and say, "If a person has these risk factors and obesity, look at the benefits we can get from this treatment. How much does a stroke cost? A heart attack? Dialysis?"

Q. Are the beneficial effects observed on the kidneys and cardiovascular system solely a consequence of reducing obesity? Or are there other mechanisms?

A. In our lab, we've been studying how GLP-1 works for decades, and it's very clear that its benefits aren't just due to blood sugar control or weight loss. How do we know this? We can conduct experiments on animals without diabetes or obesity, or monitor the weight they lose, and still see positive effects on the heart, kidneys, or liver. We published in 2009 that GLP-1 drugs can reduce heart attacks and improve heart function, even without weight loss or diabetes. And now, finally, we have clinical evidence.

In the SELECT trial, which included more than 17,000 people with obesity and heart disease, a 20% reduction in heart attacks, strokes, and deaths was observed, and those who lost less weight saw the same benefit as those who lost more. So it's not weight loss that's driving the benefit.

A few weeks ago, at the European Congress on Obesity in Spain, results from another Novo Nordisk study on metabolic liver disease with semaglutide were presented. Researchers showed that the benefits to liver health (less fat, less fibrosis) were independent of weight loss. Even those who didn't lose weight experienced similar improvements. So there's growing evidence that many of the benefits of these drugs aren't dependent on weight loss. That's not to say weight loss isn't good. It's fantastic! It improves inflammation, joints, the whole body benefits. But the additional effects of GLP-1 go beyond weight loss.

Q. Sometimes, the benefits of these drugs and their few side effects seem too good to be true. There are diabetes drugs, such as metformin, that could be used to slow aging. Do you think the same could be done with GLP-1s?

A. There's a lot of interest in using GLP-1 for aging. But conducting rigorous clinical trials on aging is very difficult. Studying people for 15 or 20 years takes a lot of time and a lot of money. That's why the aging science community is trying to develop what we call biomarkers—indicators of aging in cells, tissues, and blood—that can be measured easily and noninvasively over one, two, or three years and see if they predict a slowdown in aging.

But there are also people we call the worried well —healthy, but older people who don't want to leave this world prematurely—who are already taking metformin, GLP-1, or rapamycin. They're not going to wait 5, 10, or 15 years to find out if it works.

The aging science community is very interested in GLP-1, both for its effect on weight loss and its ability to reduce inflammation, which appears to be closely involved in the aging process. So the interest is enormous, although the science is still in its early stages.

Q. I assume that many people in the medical or scientific community are already taking these drugs, as was the case with metformin .

A. I don't know the numbers. I suppose Novo Nordisk or Eli Lilly would know how many people have a prescription without being diagnosed with diabetes or obesity. They would know. We don't.

We can divide people into two very simple groups: some eat to live and others live to eat.

Q. Improvements have also been seen in people with addictions. What does this tell us about the mechanisms at play? How can something that helps with obesity or cardiovascular health also help control urges for other substances?

A. If you're wondering where in the body there are the most GLP-1 receptors—because that's how it works: it binds to a receptor on the cell—the answer is: the brain. There are many regions of the brain with these receptors. And if we're talking about food again, why do we eat, in simple terms? We need energy to survive.

We can divide people into two very simple groups: some eat to live—food doesn't matter that much to them, but they know they need calories to get through the day—and others live to eat, because eating is social, pleasurable, and excites them. And many of us are in between. If you have ten friends and you go out to dinner on a Friday, some will say, "I'm not very hungry, but I'm going because we're going out," and others will say, "That restaurant has my favorite paella; I can't wait to try it again!" So, clearly, there's a hedonic pleasure in food. We all have favorite foods that excite us. And addictions also have that pleasure component. Why do we smoke, why do we use cannabis, alcohol, or narcotics? Because the use of those substances activates a reward system in the brain.

What GLP-1 seems to do, whether it's someone who loves paella or someone who smokes, consumes alcohol, or consumes cannabis, is reduce the level of pleasure they get. It makes people say, "I'm not that interested in dessert anymore," or "I don't need that extra cigarette or that extra beer." It's like there's nothing exciting about it anymore. Before, there was enthusiasm, brain activation, desire... And now, not so much.

This is a simplified explanation, of course, but there are shared biological mechanisms that regulate our response to food cravings, as well as to other substances or behaviors. And GLP-1 appears to attenuate those reward pathways.

Now, in the case of substance use disorders, this science is just starting out. We don't yet have rigorous data that says, "After six months of GLP-1, smoking or alcohol consumption is reduced by 50%." We don't know. What we have are very small studies, and many testimonials: people who took it for obesity and say they stopped smoking, that they drank less beer... But we don't yet have strong scientific evidence to say, "This works for 40%, 50% of people," or if it only works for 5% or 10%.

Q. Do these drugs reduce excessive desire?

A. There's a very wide range of responses. If you talk to a lot of people, you hear everything. From: "I'm not hungry, but I'm fine," to "I'm not hungry and I feel a little tired," to "I'm a little sad." And then there are those who say: "I'm depressed, I have no motivation, I don't want to do anything." I think most people feel fine, but if you treat enough patients, you'll find some who say: "This medication makes me feel apathetic, sad, depressed. I don't feel like doing anything anymore. I don't like how I feel."

Q. Do you think that, given the safety levels we've seen, it would be reasonable to give these types of medications to people who aren't sick or who we don't define as sick?

R. Do you mean using them only for weight loss?

Q: Yes. Or perhaps also to regulate desire in people who feel they are consuming too much of something.

As a scientist, I would never suggest that we stop investigating the causes of obesity.

A. I'm a scientist, and I'm very conservative. I always remind people that we don't have enough data on many different types of people to clearly understand what safety is and what benefit is. If someone said to me, "I want to know if it's safe to treat people who don't have type 2 diabetes or obesity, but who want to lose 10 kilos because they would feel better if they could get back to their high school weight," I would say, let's do a clinical trial. Take 5,000 people with a BMI between 25 and 28, treat them for six to twelve months, and see if the risk-benefit ratio is favorable.

Personally, I'm not too worried because we've been using these drugs for 20 years; they're not new. But as a scientist, I'll always say that you have to study the population you want to treat, not simply assume that everything will be fine and there won't be any side effects. I'm very conservative: I don't sell drugs, I study them.

Q. Do you see a risk that, in 20 or 30 years, we'll simply stop trying to prevent obesity or diabetes—and all the associated problems—and opt for taking drugs and forgetting about the root cause?

A. I hope not. I think that would be a missed opportunity. We shouldn't approach the problem of obesity through treatment alone. We should always strive to understand why the problem develops. Because what if the solution is very simple, very easy, and very cheap? That would be much better than taking extremely expensive drugs for billions of people for years. As a scientist, I would never suggest we stop researching the causes of obesity.