The Decibel - Skinny, Inc. part 1: the Canadian connection to Ozempic

Episode Date: February 23, 2026

Dr. Daniel Drucker’s research helped pave the way for Ozempic, the blockbuster GLP-1 class drug. The endocrinologist has been researching the effects on Ozempic’s active ingredient semaglutide in the body for decades.Today he’ll show us around his lab and explain how a stout lizard kept in a freezer helped unlock the science behind a drug taken by more than a million Canadians.  Then, health reporter Kelly Grant tells us about rising obesity rates in Canada, and we’ll hear from a doctor who prescribes GLP-1s— and a patient who takes them.  This is part of a three-part series. The next episode is next Monday, March 2nd.  You can contact the National Eating Disorders Information Centre at their toll-free hotline at 1-866-NEDIC-20 or visit their website. Questions? Comments? Ideas? Email us at [e-mail] Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

O-Zempec has been the highest-earning prescription drug in the country for the last four years. With over a million Canadians taking these drugs, the globe wanted to explore what it's changing, from business to science to how it's reshaping our culture and our bodies. Azempic and all the similar drugs like it, like Wagovi, are really blockbuster drugs. Like, there have not been a drug like this in a generation. Often a patient will come and they'll start off, I ask them why they're here, and they'll say, I've tried so hard, and they start crying. It's the best feeling, honestly.

I look in the mirror and I'm like, oh, yeah. Not everybody considers obesity to be a chronic disease, but most major medical organizations do. I think that there's understandable lack of trust. Like, can I still work on body acceptance? Side effects. Nausea, vomiting, diarrhea, constipation, slowing of gut mortality. For the next three Mondays, our special projects producer, Kasha Mihailovich, is going to lead us through it all.

And Kasha is here to give us an overview. Kasha, thanks so much for joining me in studio. Thanks for having me, Cheryl. I can't wait to tell everyone about glucagon-like peptide-1 receptor agonists. Okay, so that's probably a very good place to start because there's a lot of terminology to learn when it comes to these drugs. So what are you talking about? So that's the full name of GLP-1s. the class of drugs that now include Ozempic and Wagovi and Manjaro and Zepbound, and there's even more.

But those are the big ones. Okay. And just so we're clear, these are the drugs that treat diabetes and also make you lose weight. How exactly do they work? On a very basic level, GLP1 medications mimic a naturally occurring hormone called GLP1. That's what manages partly our blood sugar and tells us when we're full from eating. but researchers are actually still trying to figure out all of the illnesses that GLP-1s can treat and how exactly it works in the human body. And you spoke to a lot of people over this three-part series.

So can you give us a brief overview of what we're going to hear? Well, you're going to hear from our colleagues, people like health reporter Kelly Grant and business of health reporter Chris Hennay. You'll hear from some of the people using these drugs and from leading doctors and scientists, including one man who's been researching GLP1. once since long before OZempe came around. And who happens to have a lab right here in Toronto. That's where we'll start.

Okay, that sounds great, Kasha. Take it away. Thanks, Cheryl. I'm Kasha Mahalovich, and this is the Decibel from the Globe and Mail. I was just really fascinated by the idea that we have these drugs. They seem to do a fair amount of amazing things. But despite all that, we just still didn't have a great grasp of exactly how they did all the things they did. That's Kelly Grant. She's a veteran health reporter and has done a lot of the reporting that's gone into this project.

So I've been covering health for the globe for 10 years now, a little over 10 years, actually, and I really love it. To understand the science behind GLP1s, Kelly went straight to the source. I was fascinated by the guy who helped develop these decades ago, still wanting to work to unravel the mystery of how these drugs actually work in some. the human body. And the guy she's talking about is Dr. Daniel Drucker. He's an endocrinologist, which is a doctor who specializes in hormones. He's also a pioneer in GLP1 research, and we went to his lab at Mount Sinai Hospital in Toronto. It looks like what you think, with the crowded workbenches and the glass beakers and all this equipment and scientists and lab coats. We're in Dr. Drucker's office, when he goes into a cupboard

and brings out a bottle of tequila named after a poisonous lizard. So this is Gila tequila. So the first GELP1 medicine came from a lizard venom. So I did not discover the lizard venom. The credit goes to John Ng, who was a biochemist who worked

at the Bronx Bay Hospital in New York. Drucker then tells us a very condensed history. of how drugs like Ozempic were first developed. He'd been studying GLP-1s since the mid-1980s, before Dr. Eng discovered that the Gila monster's venom made something called Excendin 4, a molecule similar to the gut hormone GLP1

that we make in our bodies. And he was just randomly looking for new bioactive substances in the lizard venom, because when reptiles bite you, you know, things happen, right? you can either die because they inject an anticoagulant into you. If it's a frog and they kiss you, you'll turn into a princess. So people have looked for medicines in snake venom and reptile venom and frog secretions. And so he found this protein that looked sort of 50% like JLP1.

And he said, oh, this was really cool. I wonder if I could use this to treat type 2 diabetes because it seemed to be a little more resistant to breakdown. you help you want. And Drucker says Dr. Eng could not stop talking about this. You would go around to everyone saying, I've discovered a protein from the venom of a poisonous lizard. When this lizard bites you, you become extremely sick and you might even die. But one of the proteins in that venom, I think might be really cool to treat type 2 diabetes. So he patented that. The Bronx VA, where he worked, did not want to help him patent it because he thought he was a crazy person.

So they just dismissed him out of hand. But Drucker also became, I think it's fair to say, obsessed with the lizard venom. He wanted to study it. And in order to do that... I had to get a lizard and clone the jeans. I still have the lizard in the freezer, actually. Now she's excited. It's true.

Kelly and I both lit up. I could not part with the lizard. I still have this lizard from 1990s. Sadly, only our photographer Sammy Cogan got to see it. And he said it was maybe a little bit frivolous. freezer burned. It has these like orange bumps on the top and you start to see that it really is just like a

foot long frozen lizard that's at least a couple decades old from what I'm hearing. Yeah, that's a 20 year old frozen lizard. That's a 20 year old frozen lizard and it doesn't look a day younger. Actually it's more like 36 years old, but anyway, Dr. Drucker clones

some of that hila monster's genes to better understand what this GLP1-like thing extended four is. And that work, after many, many years paid off. Drucker's cloning research was licensed to a pharmaceutical company, and they made the first GLP1 drug called Exanatide. It was approved to treat type 2 diabetes by the American Food and Drug Administration in 2005.

That was one of the most exciting days of my life. Because something you work on in basic science has like a 1 in 10,000 chance in becoming a drug. despite the press releases and all the, you know, hope and hype that we have. But what did you see that other people didn't see it? Well, you have to remember, like 25 years ago, none of us had ever heard of GLP1. We didn't know what it would do. If you said, oh, it stimulates insulin secretion, they would say, well, we already have pills that stimulated insulin secretion. We didn't know about the weight loss.

We didn't really know about the potential. So no one cared for the first couple of decades. And you cared why? Because I started with the story in the 1980s, and I thought it was pretty cool, and we just kept plugging away. And in the 40 or so years, Drucker has been plugging away. He and other scientists have discovered new ways to use GLP-1s by understanding more about how they work in the body. In some cases, we know that if you have type of diabetes, the medicines lower your blood sugar. if you are living with obesity, the medicines lower your body weight.

And those actions in turn, over time, make you healthier and maybe make you less susceptible to heart disease, to liver disease, to kidney disease. But losing weight and lowering blood sugar are only part of why Drucker thinks GLP1 can improve our health. It also seems to help reduce other risk factors that can. contribute to health problems. For example, JLP1 lowers your blood pressure. We know that JLPOM introduces heart attacks and strokes and neurodegenerative disease

and having high blood pressure is bad for all of those and it was a risk factor. So that might be one additional benefit. JLP1 seems to affect your coagulation system. Coagulation means the way your blood clots. JLP1 seems to lower your circulating levels of blood fats. that can lower your cholesterol. And, you know, inflammation is another risk factor for these complications. And JLP1 does lower inflammation in many settings.

So there are all these risk factors that JLP1 modifies. And we don't fully understand how JLP1 does that. And so that's a big part of what we do. And then, you know, there are receptors on all of these organs that JLP1 seems to help. These receptors are how JLP1 makes. medications get their full name, glucagon-like peptide-1 receptor agonists. On a cellular level, GLP-1 finds each receptor on each cell and basically tells it be healthier. And there are these receptors for GLP-1 in the kidney, in the heart, in the blood vessels, in the brain, many different places.

And we think that there's a direct contribution. All of this is exciting because it shows that GLP-1 medication helps people, in a variety of ways, not just by losing weight, as many people have thought over the years. So it's a combination of improving your metabolic health, reducing your risk factors for chronic disease, and directly talking to those cells in those tissues to make them healthier. So, GLP-1s are communicating with different parts of the body. But how do GLP-1s make people lose weight? That, interestingly, is all in the brain, according to Dr. Drucker. And he knows that that in part because of what he's seen in mice when they remove the GLP1 action in their brains.

You took the GLP1 receptors out of the mice's brains, and then that stopped the weight loss. Yeah, we inactivated. Yeah, inactivated, right? So does that mean that, like, we are now, or you are now certain that the activity that leads to weight loss is centered in the brain as opposed to the brain and the gap? You think it's 100% in the brain? It's always been 100%. Because, you know, you read a lot about how the, you know, OZepic stops stomach emptying or slow stomach amput. So it's a very common misconception even in very smart scientists.

I'll show you the paper that we just sent back. Here, Dr. Drucker pulls up a paper about what GLP-1s do in the brain that was sent to other scientists to read before it's published. This is called peer review, and it's an important process for good scientific research. And once those scientists have reviewed the paper, then Dr. Drucker gets to respond. And I try and be polite, but I don't want to be like that. Nasty guy. A reviewer three, remember, these are all like experts in how GLP1 works. Okay?

So here's the first comment reviewer three makes. You need to revise some statements for accuracy. For instance, authors say that GLPO effects on gastric emptying the way our gut, is empty motility are central, but there are also peripheral mechanisms. And I politely say, thank you. There is no evidence that I'm aware of that GLP1 controls emptying through peripheral mechanisms. None. Okay. And so there's this misconception. So all of the GI side effects, nausea, vomiting, diarrhea, constipation, slowing of gut motility, that's all through the brain. It's been shown like without doubt, if I not get the receptors in the brain, I remove all of those actions.

Okay. So I guess the key thing for what I'm trying to explain this for a lay audience is, yes, somaglite slows stomach emptying, but it's because it acts on the brain and the brain tells the stomach to slow down? Correct. Correct. And that when you inactivate the GLP1 receptors in the brain, that goes away. Correct. Okay. Drucker is also used to correcting another common misconception. Do people wonder whether you are also like the Osempic billionaire? Like have you made money off of your contribution? Yeah, well, people ask me that all the time.

And all of the modern medicines today, you know, the patents were held by the drug companies. You know, I did clone some of the GLP1 associated genes and licensed them. And don't get me wrong. So I have had an amazing career. I have made a lot of money through my work, but I have never made $1 in licensing revenue from the sale of any GLP1 medicine. And some of my business-oriented friends are so disappointed in me, but you should not feel sorry for Daniel Drucker. Daniel Drucker's lab and labs across the world are doing amazing work to understand how GLP1's can help fight disease. But if we're honest, GLP1's rise to fame comes from its ability to make people lose weight.

After the break, we'll talk more about that. After our trip to Dr. Drucker's lab, Kelly and I sat down to talk more about GLP1's most famous effect, weight loss. first of all, what can you tell me about how many people in Canada fall into the category of overweight and of obese? And how do we know that? We don't go around measuring everybody. Well, we do actually go out and physically measure at least some people or statistics Canada does. There are a couple of different sources we have for our estimates of the rates of people who are overweight and obese in Canada. but they both come from Statscan. Statscan does something called the Canadian Health Measures Survey,

where they actually go out in these, like, tricked out tractor trailers that they've turned into kind of mobile clinics, and they travel around the country for two-year periods, bringing volunteers in to test all kinds of different aspects of their health. And one of the things they test is their weight. They ask them to get on a scale, and they also, you know, use a tape measure to, take a look at their waist circumference, hip-to-waste ratio.

Then there's also something that statscan has called the Canadian Community Health Survey where they ask people to self-report their height and their weight as part of a series of questions about their health. So what did the last version of the Canadian health measures, the in-person survey, tell us. It told us that 68% of Canadians, an estimated 68% were either overweight or obese, and that is up eight percentage points from a period before the pandemic. Now, of course, that's 68. A good chunk of that is overweight as opposed to obese.

The prevalence of obesity in the most recent round of collection was 33% for adults. And that's also up. When did we first start classifying obesity as a disease? Oh, gosh, none of these questions are going to have the straightforward simple answer that I think you're hoping for. Not everybody considers obesity to be a chronic disease, but most major medical organizations do. So in Canada, the Canadian Medical Association, which represents physicians, declared obesity

a chronic disease back in 2015. Most provincial medical societies like the Ontario Medical Association do the same thing, the World Health Organization. And the disease is defined just by what your BMI is? That used to be the crux of the definition. Now, there was some really interesting work done last year by a commission that was put together by the Lancet that wanted to try to move away from BMI and redefine how we think about obesity. They spent a couple of years looking at the research.

They got endorsements for this position from all kinds of medical societies and patient groups around around the globe. And where they landed was saying, we think that rather than looking at BMI, a better idea is to look at adiposity, how much excess fat a person has, right? Because this is what's thought to be the main contributor to many of the metabolic diseases that often are linked to obesity. And what this Lancet Commission said was we would consider somebody to have the clinical condition of obesity if they have excess adiposity, so too much body fat, right, and at least one weight-related metabolic comorbidity. Then if you have excess adiposity, but none of these, you know, diseases that are associated with higher weight like, you know, cardiovascular disease

or diabetes, they would deem that pre-clinical obesity. So clinical obesity and pre-clinical obesity. So that's where the Lancet Commission landed on that question. So yeah, you're right. If nothing is straightforward or totally simple about this, there's a lot of in between and a lot of nuance. And I think that nuance is really important, especially when we're talking about people who are living in larger bodies. You know, there's people I've spoken to who say, well, wait a minute, just because I'm in a larger body, I'm not sick. I don't feel as though I have a disease. so why would you categorize me as having the chronic disease of obesity? Now, that doesn't mean that it's going to stay that way forever, right?

And that having excess fat may in the long term still lead to developing some of these metabolic illnesses. But in the moment, that's a real contentious debate for some people who are living in larger bodies. I know that sounds euphemistic too. There's real debates about a lot of the terminology in this space that we're going to be talking about. The big question I have is why? Why are these numbers trending up? Why are more and more Canadians overweight or obese? It is the subject of a lot of debate, but I think big picture, the obesity rates had been rising

slowly over decades in Canada. And the expert consensus seems to be a combination of our food environment changing really substantially. People going from eating, you know, three home-cooked meals a day to just a litany of ultra-processed junk food. And we're surrounded by it. It's everywhere. It is cheap. It's easy to get your hands on. It's delicious. It is addictive. It's hard to say no to. And our lifestyles have become much more sedentary. We're sitting in front of computers all day as opposed to being, you know, outside and moving around. We're not sleeping as well. We spent too much time sitting on our screens. The world around us has changed in a way that's really conducive to making us gain weight.

Do you mind if I record this part? Just I'm going to look at the at the levels and see what you sound like on here. Okay. Testing. One, two, three, testing. Stephen Glazer is a doctor who specializes in treating people with obesity. We spoke. after hours at the Humber River Health Hospital, where he's the medical director of bariatrics. He proudly showed me the chairs, the bathrooms, and the medical equipment that accommodate the size of his patients before we sat down in his office, just like his patients do. Often a patient will come and they'll start off, I ask them why they're here, and they'll say, I've tried so hard, and they start crying, or they'll tell me, it didn't matter what I did,

I tried this diet, I tried that diet, I've lost, but I gained, and then some. And they really are suffering. They really are suffering. Dr. Glazer's clinic works with different treatments for obesity, like bariatric surgery, specialized programs that include lifestyle changes, and medications, which now includes GLP-1s. I believe that what we're seeing is a greater attention towards obesity. obesity because of the options that we have to treat obesity. So if I look back, you know, 10 years when I was young, first of all, there wasn't a recognition

of obesity as a chronic disease. So I think that recognizing obesity as chronic disease provides legitimacy for addressing it. But what could we do? You know, we had so many medications. If you look at the history of pharmacology for obesity medications, so many medications. So many of them were associated with very negative or very dangerous side effects, mostly cardiac, but others. And so we really didn't have a box from which we could choose to treat people living with obesity. You will agree that in the last several years, it's exploding. You know, it just snowballed.

And I really do believe that we are very much at the top of this big, big hill with the snowball right at the top and we're pushing it and it's starting to roll. And, you know, we are. helping people in ways we never, ever dreamt of? This was the easiest thing I've ever done. I call it my magic drug. It just made things so much easier. That's Virginia McKinnon. Kelly spoke with her and other people using GLP1s to hear about their experiences.

Virginia's in her 70s and lives in Sue St. Marie. She felt like using the drug helped her. lose weight when more traditional diets didn't. It takes away the cravings and the constant fight that you have when you're with Weight Watchers to not have things that, you know, when your own Weight Watchers or any of those other programs, you constantly fight to say, oh yeah, it's great. It changes how you eat and all that, but you're still constantly fighting against it. With the Wagovi, you don't feel that constant fight.

it sort of becomes a no-brainer. Virginia has tried to lose weight for years, in part to help with the arthritis in her joints. I was aware that there were going to be ongoing issues that could arise from my weight that I wanted to avoid if I could. My husband is a wheelchair user. He's quite disabled, and I wanted to be fit to be able to continue caring for him. In 2024, she started up. on Ozembek and then switched to Wagovi and lost 90 pounds in a year.

Virginia told Kelly she plans to maintain her weight by staying on GLP-1s, but that's not everybody's plan. Another person I spoke to a younger guy named Abdul, he was an example of somebody who has gone off the drug. He had a goal weight to achieve. He wanted to feel better physically and be in better shape. He lost about 30 pounds, felt like it worked well for him, and he was ready to go off of it. And so he stopped. And then I spoke to others, you know,

for whom the drug just didn't work. There was one woman I spoke with Jill Hepburn. And she went on both Ozzympic and Wagovi and just found they didn't make any difference to her appetite. And she wanted to share with me that, you know, these drugs aren't miracles that work for absolutely everyone and how hard it was to see them working so well for other people and finding they didn't work for her. And she actually had a couple of people in her close circle who'd also gone on OZempic and hadn't lost any weight. Now, that's why there are so many drug companies that are out there searching for and doing clinical trials around different versions of these drugs that target more hormones and that seem to produce greater degrees of weight loss. Think of OZemps. Think of

OZempic as very much a first, maybe second generation of these drugs, and there's many more generations to come. An example of a slightly newer weight loss drug is Tersepatide, also known as Mujaro or Zepound. It's a GLP 1 similar to OZempic. The main difference is that terseptide targets two different hormone receptors, GLP1, and another one that is abbreviated as GIP, GIP. Okay. It's like a double whammy. Yeah, you could put it that way.

That's probably scientifically what they say and why it works. It's in all of the papers I read. But even with the new variations of these medications hitting the market, like all medications, GLP ones come with some risk. Dr. Glazer pointed out one in particular. In any sort of weight loss experience, usually we see. see like 75% fat loss, 25% muscle loss, that's almost a universal observation. And loss of muscle mass leads to weakness, it leads to sarcopenia, it leads to fragility, and those sorts of

things lead to fall and falls in the elderly are catastrophic. Loss of function because of muscle weakness. These are quality of life issues. That's why, you know, with my patients, every single patient for whom I prescribe any of these weight loss medications, it always involves a conversation about physical activity and resistance training and healthy choices, et cetera, et cetera. So muscle loss is a big deal. And the more we can preserve that through weight loss, you know, the better the future is for these people. Then there's the common gastric side effects.

Here's Kelly. nausea, vomiting, diarrhea, constipation. You know, you hear a lot about the constipation. Sulfur burps, I think I've seen on the internet. Yes. Yep. So these are, they're quite common. And for many people, they lead them to say, I don't want to stay on these drugs. It's just too, they're too difficult to take. But going off the drugs has its own potential consequence. There was a recent meta-analysis, a study of studies that came out in the BMJ that, suggested that people regain weight even faster when they come off these drugs than they do when they stop a run-of-the-mill diet. So I think we do have to think about what the implications are of patients starting these drugs and perhaps having to stay on them for the rest of their lives.

Now, as I had many obesity doctors say to me while I was reporting out these stories, there are lots of drugs for chronic diseases that people stay on for decades or for their entire lives. You know, if you need blood pressure medication, you stay on your blood pressure medication. They're treatments. They're not cures. Exactly. And why is it bad to lose a bunch of weight and then gain it back? Well, you go back to the old yo-yo dieting thing, right? Like, it just seems to be bad for your metabolism to have your weight go up and down and up and down. And then it becomes even harder to keep weight off as you get deeper into that process. And there are a couple of different theories about why people stop using these drugs. One is the side effects that I mentioned earlier.

Another is that, like other medications for chronic diseases, the adherence rates are often not great when somebody is expected to take a drug for kind of ever and it isn't for an immediate sickness that you're feeling. You know, it's not an antibiotic because you've got strep throat or isn't chemo for your life-threatening cancer. Those kinds of drugs don't have great adherence rates as a general rule. And then the other reason I hear most commonly as a theory for why people stop these drugs is the cost. The cost.

It's something we don't always have to think about here in Canada thanks to public health care. But when it comes to weight loss, GLP1 medications do have a price tag. How much you pay depends on your health insurance, your medications brand, the dose you take, who you buy it from. And as of this year, how many companies start money. making generic versions of somagletide, also known as Ozympic and Wagovi. In the next episode of Skinny Inc, we'll get into the big business of GLP-1s. Thank you for listening. I'm Kasha Mihailovich. This episode was produced by me and Ali Graham. Sound design and mixing by Ali Graham. The Decibles senior producer is Adrian Chung,

and our managing editor is Angela Pichenza. We'll be back next Monday with the second episode of Skinny Ink on the Dusible.