WHOOP Podcast - Understanding GLP-1: The Latest Research from WHOOP with Dr. Greg Grosicki

Episode Date: March 12, 2025

Are GLP-1 medications the future of weight loss? On this week’s episode, WHOOP Global Head of Human Performance Principal Scientist, Kristen Holmes, sits down with Dr. Greg Grosicki, WHOOP Senior Research Scientist, to discuss all things GLP-1 and GLP-1 Receptor Agonists (RAs). Dr. Greg Grosicki is a member of the Performance Science team at WHOOP, an accomplished IRONMAN athlete, and holds a PhD in Human Bioenergetics and a Masters Degree in Data Science. Dr. Grosicki’s background focusses on exercise physiology and aims to help people live longer and healthier in order to perform at their peak. Dr. Grosicki recently led a study at WHOOP that looked into the effects of GLP-1 RAs on heart health and responses in health behaviors. Kristen and Dr. Grosicki discuss Dr. Grosicki’s journey to WHOOP and his research background (1:32), using exercise physiology to help people live longer and healthier (02:52), and how research at WHOOP will help you live better (06:07). Dr. Grosicki dives into the WHOOP GLP-1 study (10:54), GLP-1 medications access (20:48), and what people should expect from a GLP-1RA (23:09). Kristen and Dr. Grosicki break down GLP-1 RAs, their relationships with food addiction (24:30), Hollywood (26:16), and the idea of microdosing drugs like ozempic (27:10). The episode continues, providing an understanding for the importance of studying GLP-1 and using WHOOP as a tool for data collection (28:20), the study’s results (32:56), and identifying research bias (35:55). Kristen and Dr. Grosicki discuss the relationship of GLP-1 and cardiovascular health (39:07), the impact of exercise on cardiovascular health (40:28) and maintaining muscle tissue when using GLP-1RAs (43:42). Read the study here: Heart and health behavior responses to GLP-1 receptor agonists: a 12-wk study using wearable technology and causal inferenceSupport the showFollow WHOOP: www.whoop.com Trial WHOOP for Free Instagram TikTok YouTube X Facebook LinkedIn Follow Will Ahmed: Instagram X LinkedIn Follow Kristen Holmes: Instagram LinkedIn Follow Emily Capodilupo: LinkedIn

I was talking to my old postdoc advisor, Roger Fielding, who the human nutrition research center on aging, the word sarcopenia came from there, right? It means poverty of flesh. We were talking about GLP1 and his excitement for the research and all of his colleagues talking about sarcopenia and GLP1s. And the reason why is very important, right? When people take these medications, we see that they're losing a lot of weight. 20% of their total weight is being lost in a year. But we see that almost half of that weight can come from muscle. To be fully transparent, the implications of that for strength and performance and health span are not yet clear. But it still seems concerning, particularly if we think about the population who's taking these

GLP-1 medications, most of them are 40, 50, 60 years of age, which is right at the period where muscle loss is about to begin to accelerate. Throwing additional fuel on that fire is not something we would want to do. Dr. Greg Gersicki. Kristen, so happy to be here. I'm so pumped for this. conversation. We're going to dig into all things, GLP1 receptors. We recently published a paper, which you were the principal investigator and really the lead on that paper. And it really is

groundbreaking in a lot of ways. I think there's a lot we don't know about these medications. And I think the more research that is done, the more we can learn and the more we can use these medications responsibly. Just really grateful for you taking the lead. and your contributions in this space and so excited it again. First of all, you recently joined the performance science team, so I could not be happier. But tell me, you know, what drew you to whoop? Yeah, no, really a dream come true, Kristen. And thank you so much. Couldn't be more delighted to be here and work with you and the team. And I do want to say, though, maybe I was the first author. It was a team effort, as you well know. Major congrats to Finn and Jane on their first papers of

their beginning, but certainly long and productive scientific careers. And then it was a cross-functional effort, right? And that's how everything is here. It wasn't just performance science. We had summer from data science helping us out. And that's how great research is done. So it was a team effort. I think that's ultimately what drew me to Whoop, right? I have an athletic background, right? From high school to having a chance to be an athlete in college. And I do think that the really neat thing about Whoop is it really is a team atmosphere, right? And our ability to answer like this in the GeoP1 space is unparalleled and unrivaled by anyone, I think. We have access to data earlier and before anyone else can get it. And I couldn't imagine a more dream job for

someone who's interested in the physiology space. Yeah, we do get to ask, I think, really exciting questions and we're well positioned to answer a lot of those questions that have vexed the human performance space. You started out as a, you're a triathlete, professional triathlete, you have participated in Iron Man. Tell us a little bit about, you know, just how your background in athletics get you potentially interested in exercise physiology. What was that transition like? Yeah. Yeah, no, that's a great question. And I think a lot of it goes back to a conversation I had in graduate school with an advisor, Dr. Jeffrey Katula. And I'll never forget, I got into exercise physiology. I think like a lot of us do in the exercise physiology space,

I wanted to be faster. I wanted to be stronger. I want to be bigger. I wanted to be a better athlete. And yeah, it made me a better athlete. But I think that question posed by Dr. Coutula, I'll never forget. I was in his office and working on my thesis project and he said, Greg, like, you're pretty good at this stuff. But ultimately, would you rather have an athlete run a quarter of a second faster for 100 or help someone get down on the floor and play with their grandkids when they get older? And I've just walked out of his office and my mind was blown. I hadn't really thought about it. from that perspective, right? And I think that's what's so cool. As an athlete, I was very mediocre, very back of the pack competing against pros. But when you think about how you can apply your experience as an athlete and your learnings from many years of school to help someone get down on the floor and play with their grandkid or live 10 years longer and or have a higher quality of life, that's where you really realize how much of a bigger impact you can make. And

And ultimately, you know, that's my goal. And that's what I've been blessed to do. I love that. I think about that all the time. And that's, you know, when I think about my trajectory over the course of my career, you know, it's always about just squeezing the efficiency out of athletes, you know. But I think that's what's been so magical, I think, with Woop and just seeing how, yeah, we can squeeze efficiencies out of the Patrick Mahomes, of course, right? but the opportunity that we have for just the regular Jains and Joe's is transformational, right? When we see what we're able to accomplish. And I think this GLP1 study kind of, you know, highlights that when we're combining this really powerful medication with the tools and insights and coaching that come with WOOP, there's even more opportunity for improvement.

So we'll talk more about that. But I really get excited about, I think, the opportunity with WOOP to really scale everything that you're talking about in terms of, you know, health and being able to really perform at a high level when you are in your 70s and 80s, you know? And I think that's the ultimate kind of mission, really. Yeah, I couldn't agree more. And I think just like you were saying, taking what we learned from a guy, like Patrick Mahomes, right? Right. He was not only competing at the highest possible level in football, but he also has three kids, right? And he was competing in the playoffs and the AFC championships. a week after his third kid was born and performing at the highest possible level that a human has ever done, right? How can we take that knowledge and help people live longer, healthier lives, right? And I think this paper really sets the precedent for us doing that.

And how can we take whoop and apply it to all sorts of different conditions? And how can we use it to enhance people's health span, right? Yeah. I love that. It's beautifully sad. And when you take that kind of exact example in terms of, you know, thinking about. And because I think it's sometimes it's really hard for folks to be like, to make that leap between, oh, I see whoop on Patrick Bohm's. I see whoop on Cristiano Ronaldo. They can't quite connect the dots in terms of who for me, you know? And, um, maybe talk about why is whoop literally for everyone? Yeah. I mean, at the end of the day, we're all facing the

same things, right? Well, many of us are fortunate enough to have children. And so we're trying to juggle like, okay, like, what can I do actionably to improve my sleep? Is it trying to go to bed and wake up within a very close time and really focus on that sleep consistency aspect? Or how am I able to make the most of the 20 minutes I have during the day, right? And following, like, a lot of what you will post on social media and Instagram in particular about like, okay, I woke up and drove my kid to school and then worked all day and now I'm at soccer practice. Well, time to be the parent who's on the sidelines. with a kettle of mouth, danging out burpees, right? It's like, listen, don't look over at mom right now

because you're not going to like it. And right now my daughter's five. And so she loves seeing dad do that, but when they get older, but regardless, right, like how can we in our daily, busy lives, right, inject as much health promoting behaviors as we possibly can? Right. That's the golden egg. Yeah, I love that. Let's talk a little bit about your PhD and in human bioenergetics and just you have an extensive research background and you actually get your master's in data science. Talk a little bit about, you know, what motivated your, your PhD and then just your desire to kind of go back and get your master's in data science. Like, you know, those are pretty big decisions, you know, like when you were like, okay, what am I actually going to focus

my dissertation on in my research? You know, talk a little bit about, about that decision-making process. Yeah, yeah. Well, I've been very blessed to have a lot of opportunities to study from some really fantastic scholars and mentors. And so obviously that's been a privilege. Ph.D. was the human performance laboratory at Ball State, which is founded by legendary David Costel, who in the field of exercise physiology doesn't get much higher than Costal, right? And at lunch to have Costal come over and grab us and pull him downstairs to go swim with him because he was working on breaking the 80-year-old freestyle swimming record for Masters and getting to grow up and advance my scientific toolkit in that type of environment, it's incredible. And it's simple things like

he was working on a presentation, Grisicki, come over here. Here's a bunch of articles, but I don't know how to get my figures into this PowerPoint. It's like, oh, doc, we can actually find the article. I'll do that, right? But it's just an incredible experience and mostly studied muscle physiology, particularly in astronauts and elite athletes and then the other piece of the spectrum, older adults, right? And so how can we learn from people going to space some of the highest performers in the world to make an older adult muscle like that of a 20 or 30 year old? And there's a ton of lessons that can be applied. And I think that kind of set the foundation for how we can ask questions at whoop, right? How do we make people who are 50, 60, 70, 80 years old

function and have the same type of capacity that someone who is 20 or 30 in an elite athlete trying to be, right? Then from my postdoc was brought to Boston by Roger Fielding and got to study with him, particularly looking at sarcopenia and the microbiome. Then from there, had a professor position in Georgia where studied more cardiovascular health and got to work alongside Dr. Andrew Flat, who is an absolute legend in the field of Heart Ray variability. I got to meet him at University of Alabama. Oh, yeah. Yeah, it was, I think, in 2017, but it was a real highlight, you know, having read all the

HRV research and, you know, he was like the man, you know, yeah, he's so phenomenal. Yeah, and, you know, he's rare in that Andrew is one of the most, like, open and transparent and, like, kind scientists you'll ever meet, and you could just, he's the type of guy. You just want to go out and, like, have a beer and a dinner with. them because, yeah, very sharing and so really learned a ton about heart rate variability from him. And so I attribute a lot of my success in that field to working with Dr. Flat. And a lot of his research really in some ways inspired, you know, a lot of our algorithms and kind of how we thought through it.

Yeah. And then now obviously I'm here, but I think that's kind of the cool thing about like my career from an academic. There were a lot of different avenues I went down and kind of made me a bit of a like jack of all trades, master of none. but I think that can be kind of advantageous, right? Because we do need to be broad. We know that there's not one particular ticket to having the best possible and healthiest possible life we can, right? It's the being able to understand the vast body of literature and say, okay, like, how can we optimize health through things like sleep and activity and other health-promoting behaviors that people haven't even really begun to investigate in their novel, which is what we're

able to do. Yeah, all right. Let's talk about the study. Yeah, we'd love to. Okay. There's a lot of different entry points, but I think probably the most important is to just set the stage on what is GLP1, just give kind of an overview of this, the class of antagonists, because I think it's important just for people, because there's just so many different names. I think, you know, Shazepotide and semi-glutide is kind of how I bucket them, but I think the landscape is getting, you know, there's more and more kind of coming on the market, like how I thought about it a year ago is different than how I think about it now. So maybe just kind of give us a sense of, all right, where is the research right now? Yeah. And just a broad definition of what are these things and,

you know, what are they being used for? Yeah. Yeah, no, that's a great question. And I think the thing that is surprises most people when you talk about GLP1, particularly medications, right, is they weren't developed for weight loss originally at all, right? These medications were developed for the control of diabetes and particularly type 2 diabetes in case people aren't familiar. That's when people have blood glucose that gets too high. And with type 2, that's often because they're not able to bring glucose into the cell effectively. And so these medications weren't really developed for weight loss. And they do certainly induce profound weight loss. And that's what they're most famous for. But the discovery of GLP-1s, and this is, I think,

kind of surprising to most people, dates all the way back to the very beginning of the 20th century. And scientists realized that an intestinal extract actually lower, blood glucose. And that was in an animal model. I believe it was in dogs. But then in the 1920s, scientists found insulin, right? And they're like, oh, well, this is the golden ticket for treating diabetes. We'll use insulin. And insulin is great. But it can also, if you give someone too much insulin, lower blood glucose too much. And that can cause serious consequences and possibly death. And so, yeah, insulin's great for the treatment of diabetes. But there was always kind of in the back of people's minds, this GLP1, or really the early observations that this intestinal extract

lowered people's blood glucose. Well, in the 1950s, scientists found that when someone ingests carbohydrates orally, it actually leads to a greater insulin response than if you were to inject it. And while they weren't totally clear on what to make of that observation, what they did realize is that, okay, this at least suggests that something to do with the ingestion, the oral intake of carbohydrates is leading to something coming from the gastrointestinal tract, probably the intestine, that is increasing insulin. Now, insulin is produced in the pancreas, right, and the pancreas senses glucose levels. And when glucose gets high, the pancreas secretes insulin to bring glucose back down to kind of our resting, healthy

levels, right? But now they're observing that there's something going on in the intestine that's leading to more pancreatic insulin production. And absorption in the intestinal track. Particularly, yes, when food is ingested and it goes into the intestinal track, for whatever reason, leads to a greater insulin response than if it's injected orally, right? And so that really sparked the search for what was called incritons. And incritons were the name of these hormones that were lowering blood glucose through that greater insulin response, but no one really knew what they were, right? It's like, well, there's these incritons, and they exist, and they're lowering blood glucose, but where are they produced and what are they called and why? And scientists and drug

companies knew that if we can find these incritons, then we can have a meaningful impact on, you know, people with metabolic disease and with type two diabetes, but they didn't really know where they were, right? And so they do a bit more discoveries. And then in the 1970s to 1980s, they start to figure it out. And so going back, we talked about insulin is produced in the pancreas. Well, there's another hormone produced in the pancreas known as glucagon. And so insulin and glucagon kind of have these opposing forces. When blood glucose is high, the pancreas secretes insulin, and that helps lower blood glucose. Well, when blood glucose is low, we haven't eaten for a while, a healthy pancreas will secrete glucagon.

And that tells the liver to break down its glucose stores, which are known as glycogen. And that helps maintain normal blood glucose levels. we all know we want to maintain our normal glucose levels. We know what it feels like when they get too low, right? And so we knew glucagon comes in the pancreas and does that. What it was realized was that the glucagon gene actually is expressed more than just in the pancreas. And as a matter of fact, it's also expressed in the intestine. And the protein product that comes from that intestinal expression of glucagon isn't the same as conventional

glucagon. And that was actually evidence of this glucagon like peptide, right? And now we're getting into the realization of GLP1, which stands for glucagon like peptide 1. And there were two of these incritons, right? One was this glugon like peptide or GLP1. And the other one was one known as gastric inhibitory peptide or GIP. And so scientists found these. This was in the 1970s, 1980s, and they were off to the races. It's like, okay, we found these hormones that are increasing insulin and can have a meaningful impact on these people with diabetes on their lives. So, you know, the easiest solution to this would be simple, right? We give someone GLP1, their blood glucose goes down. Well, not so easy, unfortunately, because GLP1 has a very

short half-life, about two minutes. So, you know, we could give someone GLP-1, but in two minutes, most of it's going to be gone. It's not going to have much of a physiological effect, right? And the reason why that is is because there's another enzyme in the body called DPP4, right? And DPP4 degrades GLP1. So pharmaceutical companies say, okay, let's make a, let's make a drug that targets this DPP4 mediated degradation of GLP1. And those drugs went into market. They're known as glyptins. And they do elevate GLP1. They were approved by the FDA for managing blood glucose. And they were effective. They had efficacy for people with diabetes. So, so that was great. But when we look at these, you know, DPP4 media degradation of GLP1s and blocking those DPP4s, we still see that

GLP1 is only elevated for maybe one to two hours after someone takes one of these DPP4 inhibitors, right? Really, the drug discovery process has been all about iterating on how can we make GLP1 go up, stay elevated for longer periods of time, and how can we increase its quantity, right? These DPP4 inhibitors, maybe it's up for two hours after, okay? And a lot of people, when you bring up GLP1, they'll talk about the GILA monster, right? And that's actually where the first GLP-1 that was given to humans really came from, actually. It was a scientist studying the GILA monster, and what they noticed was in the saliva of the GELA monster. They had this longer-lasting GLP-1. And so that was marketed and sold and approved by the FDA.

I believe it was in 2005 and exenetide. And it's a medication that's used to treat type 2 diabetes, and that was GLP1. And that stays elevated for longer in people's blood. And so it's having more of this therapeutic effect, right? And the pharmaceutical companies continue to iterate off of that. And I think the next big discovery was really Lyraglutide, which was approved for diabetes in 2010. But there was, and that elevated GLP-1s even more, we're talking 100-fold, maybe. But what scientists noticed, and a lot of this goes back to animal models, when they gave people

Learglutide is it had this anorexic effect that they became less hungry. And then when they even started giving it to people, they realized they could get kind of nauseous. They weren't eating as much. And they're like, whoa, people are losing weight from this stuff. And so next thing you know, 2014, the FDA approves their glutide for weight loss. People are taking it for a year, 10% reduction in body weight. This is pretty good. All right. Now the pharmaceutical companies are really off to the races. 2017, we have Novo Nordisk rolling out with semi-glutide. And that's a what people more commonly know, right? Wagovi, which is the one for weight loss, and OZEPIC, which is the one for diabetes, they're

really the same thing. Now, this is all updating GLP-1s. Mechanistically, there's really no major difference between the two. The difference is it's lasting longer in people, right? People are injecting it, and it's having effects for a week after they inject it. So it's really, the half-life is just so much longer. They're slowing gastric motility. They're introducing satiety. They're improving insulin sensitivity. They're having a whole host of other effects that were only really beginning. to discover, right? And every year, you know, it seems like these GLP-1s are being approved for something new, right? So it was diabetes and then weight loss and Alzheimer's. Neurgenitor

disease is right. Oh, yeah. Oh, yeah. In 2021 and 2022, we have weight loss, right? And then cardiovascular disease last year and sleep apnea. And like you're saying, now recent things, like possibly Alzheimer's is coming out. Another really cool study just published by the folks at Weight Watchers show people who are taking GLP1, it helped them with alcohol addiction and cessation of alcohol. So it's interacting with the brain and dopamine signaling. The extent and the possible benefit. Cravings. Yeah, just cravings. Generally, right?

Yep, yep. And so that's kind of a, you ask a short question, I give you along. But I do think when people think about GLP1, say, oh, it's very new and very scary. And it kind of is in a way. But also, you know, people were taking these things and trying to elevate them back in 1990s, and we've known about them since 1900. So when we look at diabetes in America, type 2 diabetes, one out of every 10 Americans have type 2 diabetes, which is kind of wild. Do we know what percentage of Americans are on, who have diabetes, are on one of these GLP1? I'm not sure about that. I do know the, you know, GLP1 use is growing quite crazy as well, right? A study published by the KFF polls, I think, showed that one in eight U.S. adults have taken a GLP1 at some point.

And in adults who have been told by a doctor that they have overweight or obesity goes up to 20%. And if you consider these drugs are extremely hard to get, very expensive. We should talk about that for just a second because it's really interesting. It's like $1,000 a month. And when they look at the data on why people go off these drugs, it's very interesting. It's not because of the side effects, which I want to talk about. It's because of the cost. So that's also, I think a really interesting and important data point around from a side effect perspective, that it's not, that's not what is deterring people from continuing these drugs. Yeah, no, for sure.

Cost is, I think, definitely a huge reason people are discontinuing them. And if you look at the discontinuation numbers, they're quite high. I just published a study in diabetes, obesity, and metabolism that actually looked at that. And of people who are going on GLP1 drugs purely for weight loss, and this is real world observational studies, so we're not talking about when they're getting the drugs from one of the pharmaceutical companies, over half of them are stopping before a year. And that's not how these drugs are intended to be used. So that's a problem, right? We have a mismatch between how are people actually using these drugs and how are they intended. what's up folks if you are enjoying this podcast or if you care about health performance fitness

you may really enjoy getting a whoop that's right you can check out whoop at woup dot com it measures everything around sleep recovery strain and you can now sign up for free for 30 days so you'll literally get the high performance wearable in the mail for free you get to try it for 30 days see whether you want to be a member and that is just at whoop.com. Back to the guests. Maybe just outline what people would expect. And maybe who would benefit? You just gave a laundry list of the different effects or impact of these drugs on cardiovascular health and potentially brain health and metabolic health, obviously, well known. For folks who are wondering if they meet the criteria, what would be that criteria and what would

people expect to happen once they go on these drugs? For managing excess body, mass, the criteria are simple. You either have to have a BMI of greater than 30, and then your doctor's able to prescribe it for you. Or if your BMI is in the, and that's classified as someone who has obesity, or if you're in the overweight category with a BMI of between 20 to 27 to 30, and you have one cardiovascular or metabolic risk factor, right? So BMI of 28 and high blood pressure, then you're able to be prescribed these drugs. And when we look at weight loss, with the newer medications. So we're talking semi-glutide and transepitide, which the ones for weight loss would be Wagovi and Zep bound. A year after taking these medications in the clinical

trials, people are losing about 20% of their body weight in 12 months. It's life-changing. We're getting results for weight loss with these medications that parallels what we're seeing with bariatric surgery. Yeah, I think the addiction piece is really, really interesting to me, you know, because I think it's cravings are tough, right? And modern society isn't really set up in a way to protect us for many of that. You know, it's just so easy to get food. Oh, as a matter of fact, it facilitates it. It facilitates it, right? And so we're kind of like handicapped, not to create a lot of excuses, but it's hard. Like, I think being a human in this world of abundance, right? And it sounds so counterintuitive and it sounds ridiculous almost when I say it. But I think that's

kind of the crisis that we're in, right, is we have access. I mean, the food industry, that's a whole other conversation. I've just messed up the food industry is in access to all these processed foods, which are contributing to this epidemic. But I think at a, at a foundational level to have something that can help people with cravings, I think is, is transformational. Maybe talk a little bit about willpower. Yeah, no, certainly. You know, there's a big discussion, I think, in society at large about these GLP1 medications, right? And you see people, well, how about lifestyle? Like, how about we teach them to sleep better and to eat better and to do some exercise, right?

It's like, well, how many years have we been telling people you need to sleep, eat, and do some exercise, right? And the truth is, it doesn't work. If it would have worked, it's worked already. And that's not to say it can't, but there's certain people, right, and particularly people who have obesity, which is a chronic condition. And it needs to be treated as such for whom these medications are a life raft, right? This can literally pull people out of people don't lose weight. Just lifelong struggle for most of these folks. Yeah, it's chronic.

And this medication is transformative for them. And just like you said, because it's an addiction. It's a chronic condition. Talk about the folks who are using it. You know, I see a lot of Hollywood celebrities who are all of a sudden really skinny. Talk about what's happening there. Yeah, there does seem to be a lot of off-label use of it, right? We see it in the papers.

you know, it hasn't been approved for that. And so endorsing something like that would be extremely challenging. That being said, there's been a lot of research on GLP1s over the past 20 years and not a lot of negative findings so far. So it does beg the question of where the future of this space is going to go. And when you look at, you know, the upcoming studies from these big pharmaceutical companies, they're doing some very exciting things from right now people are having to inject themselves weekly, right? Can we extend that to a month? Can we take a pill? Right. Another big obstacle. People don't like injecting themselves and who's to blame them, right? And so to think about where this may go in the future, it's exciting and scary and it's just, yeah. So in the functional medicine space,

you know, this is being added to the stack of modalities, essentially, which is kind of insane to me, but like, micro dosing basically, Ozempic. What are your thoughts on that? You know, it's my doctor actually brought it up with me, you know, like, is this something you want to try? I'm like, I don't think so, but you know, but I think in terms of longevity and everything, you know, we think about like neurogenital disease if you're predisposed to that or, you know, cardiovascular risk. Like, is there space for a healthy adult who is doing all the things to be microdosing? We certainly don't know, but I certainly wouldn't dismiss the possibility, right? If I'm not mistaken, I believe I saw something the other day that what needs to be next checked out is using this for athletes as a, as a, as a, a doping protocol, right? We think about athletes where weight is a big piece of... That's where I was going. I mean, wrestling and cycling and I mean, boxing. Do you say that people

can't use these types of things? And then if so, how are you detecting it? It poses a lot of problems. It is an exciting time, I think, in the human performance space. But yeah, there's a lot of unknowns in that area. And that's really, I think, what, I mean, for us, we're, you know, we're investigating the unknowns all the time, right? We're going into our massive data set and be able to ask these interesting questions. Talk about how our research, you know, kind of came to be around this topic and, you know, just tell us the journey that led to this recent publication. Yeah. So, you know, as scientists, we're always looking at the literature. We're following trends. And one of the things about me is I'm following trends all over the place,

which I sometimes get critiqued for. But other times it leads to things like this, right? But ultimately, I think, you know, the idea for this paper came from one of our team meetings, right? And we were sitting around one day. And I think maybe it just started with a question. And it was me asking Finn. One of the wonderful things about whoop is we have this behavioral tracker. And so people can log everything under the sun from a nice bath to taking magnesium to sharing your bed with a dog. And so I thought, well, Finn, are we asking anybody questions about taking weight loss medication? Sure enough, we were. Now, it wasn't specific in the slightest. And this was, you know, a while back now. It wasn't specific, right? It was just, are you taking weight loss?

medications, yes or no? And I was like, oh, this is really exciting, right? And I'm talking with Finn. I'm talking with Jay. I'm talking with you, talking with Bill and Chris, everyone on the team. It's like, well, what if we were able to look at the users who have selected that they've taken these medications? And then send them just a brief survey, really, a short survey. What medications are you taking? Does it happen to be a GLP1 medication? And if so, would you be willing to share some of the data from your weight loss journey with that medication, right? Simple things, like, did you weigh yourself at four, eight, and 12 weeks after you started using these medications? Things like that. Well, we sent that survey out, right? I think another one of the cool things about members love

helping us. And so we have to be grateful for that, right? I know. We'd love you so much. Thank you. No, but seriously, right? They respond to the survey, which really unlocks our ability to figure these things out, right? And so a bunch of them got back to us and said, yeah, I am taking these medications and this is how much weight I've lost on the journey, right? So we were able to go back in their data, look at, okay, what day did you start taking these medications? How much weight have you lost? And then, you know, the thing with these pharmaceutical companies is they're very good about publishing about how much weight people lost and did they get diabetes or did it prevent them from getting diabetes or did they die. These are all great things and they need to be known,

but the pharmaceutical companies aren't in the business of talking about lifestyle, right? They make no money from it. And one of the things about whoop is we know not only what you're, not to be creepy, right, but you know, your heart rate and your heart rate variability and respiratory rate, your temp, body temperature, all these things. But we also know literally, if you're using the device as you should, what you've done every second of the day. How much you're exercising, how much you're sleeping, when you're going to bed, when you're waking up. I mean, the data just are never ending. Exactly, right? And so we're able to look at these data. Honestly, of course. Yeah. Yeah. We don't know their names, but thank you to them. For 12,

weeks, every second of what they've done, how much they've moved, what their heart rate is, and to answer the questions that for a clinical trial would take hundreds of millions of dollars and probably two or three years. And so that's where, you know, we really got excited. It's like, okay, we have these members who have been using these medications. We know what their biometrics look like. We know what their activity has looked like. And then we were able to leverage, you know, some more data science and statistical techniques to basically take the members who were taking the medications. And for every one of them basically identify their virtual twin in our database, right? The great thing about having so much data is if we have a male who's

5 foot 8 and weighs 235 pounds and has a resting heart rate of 70, and we can say, okay, let's find another one, but this one needs to live over here and didn't take a GLP1 medication. match. And so for every member who is taking the medication, we're able to basically find their twin who wasn't and set up through this type of technique, not a randomized control trial, but one that's almost as powerful. And that's what ultimately we're able to do with this study. That's such a great setup. It's so funny, just as you're talking, I get so excited. I'm like, I can't believe we get to do this every single day, you know, this type of this type of research. Huge shout out to our members who replied to our questions and, you know, gave us this really, I think, valuable data that

allowed us to pursue this question with such rigor, I think, and, you know, what ended up being a really beautiful paper. Why don't we talk through the results? What do we see and why are they important? And, you know, how can we make broader recommendations for folks who are considering these drugs? Yeah. Yeah, now it's our time to give back to the members, right? Yeah, exactly. Yeah. Yeah. And this is where, like, where you're having our meeting the other day, and I was going to show you some data. Like, I'm like, hold on, I've got to get some water. It's like, it's like, Christmas, right?

I know. We're like, I need to get settled. Yeah, I know. It's like, before I push the code, I'm like, okay, like, Grace is at school. Like, I've had lunch. Like, okay, let's like see what this looks like, right? Like, it is like on rat, being like Christmas every day. And I think the first question that we were able to answer from this is what does weight

loss look like in the real world with these medications. The pharmaceutical companies are great about publishing what weight loss looks like in this very tightly controlled site. But like you said, in the real world, it can be very different. And so we looked at self-reported weight loss among our members, right? And what we observed is that in 12 weeks time, self-reported weight loss was 10% of their original body weight. 10%. How does that compare to clinical trials? Yeah. I mean, you know, you'll look at the data from semaglutide and transepatide. And it's six, eight, maybe nine percent. But truth be told, numerically, the number was higher in our number. Yeah, yeah, it is. It really is. And the other thing

is that all the members who were taking the medication, 90 percent of them who provided a weight at 12 weeks lost more than 5 percent of their body weight, which is clinically meaningful. It means that improves their likelihood to live longer, healthier lives. right, in 12 weeks. And in the big clinical trials, this is what we're seeing the 90% 5% of weight reduction in a year to a year and a half, right? And we're seeing that in 12 week. And so then, you know, okay, chicken or the egg. So basically what the amount of weight that folks are losing in a year in a clinical trial is the same as what Woot members are losing in 12 weeks roughly. Yeah. Yeah. Let's say it this way, right? The amount of folks who are

reaching this clinically significant weight loss is the same that we saw in 12 weeks, right? And And there are nuances of how these GLP-1 medications work, which is they promote a lot of weight loss initially, right? In the initial 12, 16, 20 weeks, people lose a lot of weight. But the truth is, and these data are just coming out now, their data showing what happens if people take these drugs to three or four years? And after a year, they stop losing weight. They don't lose any more weight.

It takes basically continuing on the drug medication, and we talked about what that's costing for them to just to maintain the weight they've lost, right? And I think one thing, before I forget, right, we should all just be very upfront about is when the FDA approved these medications for weight loss, it approved them in conjunction with physical activity and a reduced calorie diet, right? And we can't beat that drum enough. It approved them with increased physical activity and a reduced calorie diet and is not just saying, just take these medications alone.

The one thing that I think we also should point out, just because I think we're, we always try to be as honest as possible, you know, folks who are on whoop, there is a kind of a user bias that we should probably talk about. They might be slightly more motivated, right? They might have more resources. Who knows? But maybe just talk through that because I think that's a really important point. Yeah, that's a good caveat. It's important to be honest here, right? First, the weight loss is self-reported. There's going to be a bias there. People are going to be more likely to want to share their weight loss if they've lost more weight. And then, yeah, again, people who are willing to partner their weight loss journey with whoop might be more motivated to lose weight, right? It also very well may be that

buying whoop is helping facilitate the FDA's recommendation to increase physical activity and follow a reduced calorie diet, whether that's through our coaching or just looking at your wrist and knowing that someone's watching. In the end of the day, you have to be held accountable. We don't know. And those are certainly things we need to look at in the future. When we zoom out, though, and we think about a weight loss journey, a weight loss journey without considering exercise and sleep in parallel, you're missing a big piece of the puzzle. So there's no surprise that there is some sort of kind of acceleration in weight loss when people are just conscious of their sleep and activity levels.

So I think it's a cool, I think, moment for a who, you know, to, you know, where we have just really been known for elite athletes and, you know, kind of professional athletes really maximizing, you know, and calibrating their lives around these data points. Like, there is no question. And we've been saying this for years and years and years that, you know, whoop is really for everyone, right? Anyone who is on any type of journey where they're trying to extend their life, trying to be as healthy as possible, extend their health span, you know, Woop is just the ultimate partner in that journey, right? Because you're zeroing in on everything that is foundational, right? If you're layering GLP1 on top,

of crappy sleep, not enough exercise, you know, not getting into the weight room. Like, it's just, it's a house of cards. You've got a foundation that has cracks in it, right? And you're layering inefficiency really on top of inefficiency. But when you deal with this foundation and you're proactive about the foundation, you know, I think the results really show that you can make more gains, right, when you're layering these modalities on top. Yeah. And I mean, we can't ignore, you know, the starting place where we talked about do people take these medications and how long do they take them, right? And we said that half people who take them in the real world are likely to stop by a year. And the data are very clear on what happens if you stop

taking these medications. And pharmaceutical companies have published it. And you stop taking these medications. And in a year, people on average have gained two thirds of the weight they lost back. So, you know, we don't know for sure, but it seems very logical that the only way to keep that weight off would be through exercise and health behaviors and sleep. Right. And so you can go on these GLP1 medications and lose that weight. But at the end of the day, the rubber meets the road, you've got to have some sort of lifestyle behaviors to support this weight loss long term. When you look at GLP1 use and cardiovascular health, you know, when you zoom out, it improves cardiovascular health. Yet we see clinically significant increases in resting heart rate

and decreases in heart a variability. Kind of talk through the contradictions there and how you interpret that. Yeah, it is a bit perplexing, right? And all these pharmaceutical companies, when they have these drugs, they have to do these cardiovascular outcome trials to look what happens. And demonstrably major adverse cardiovascular events when you take these drugs go down. And for that reason, the FDA has approved them for reducing cardiovascular disease risk. So that needs to be said. That being said, it's perplexing. Because when you take these medications and in our particular findings, right, we saw that on average in 12 weeks, resting heart rate went up three beats per minute and heart rate variability went down six meters per second and that's

in the people we're looking at a significant change right resting or heart rate variability is down 10 10 15 20 percent in these individuals and resting heart rate is up three beats per minute that's that's a lot right and so right and so how do you marry those findings like yeah it does seem good overall but if i'm taking these medications with the goal of improving long-term health and living as long as i want i'm probably trying to find a way to attenuate or prevent that. And that's one of the things we were able to look at. Right. And we saw that folks who are exercising talk through that result. So the 30 minutes of exercise and people who were exercising the impact on their cardiovascular, how that changed their cardiovascular parameters. So I think one of the things that we were able to look at and,

you know, going back to the novelty of whoop and having this data is we were able to look at what happens when you take these drugs on lifestyle behaviors? And as far as to the extent of my knowledge, no one has ever done that, right? We were the first, particularly with physical activity, right? People have looked at it with drinking alcohol, but we were the first, to my knowledge, to say, okay, when you take these medications, do people change their behaviors in regards to physical activity, right? And we showed data suggesting that, indeed, people who take these medications relative to those who don't, because we were able to use this particular type of analysis, seem to increase the amount of physical activity they were doing at week 12 versus a baseline.

And perhaps that's not super shocking, but we were the first ones to show it, and it's great to have the data, right? And it could be for a lot of reasons. People have lost weight, and now it's more comfortable for them to exercise, right? Or their energy levels increased. They're sleeping better, potentially. They're more motivated because they see the weight coming off, right? Or it could have to do with the way these medications are affecting dopamine in the body, right? We don't know, but we were able to show that. And so that's really interesting. And we know, right, from a vast body of literature and exercise physiology, that one of the benefits of being physically active is that it reduces resting heart rate.

And that's a beneficial thing. And so we hypothesized going in, but had no idea whether or not we would see it, is do those who do more physical activity when they take these medications, maybe not see those changes in heart rate that we see in the regular population. And that's where it gets really exciting. We showed trends suggesting that that's probably the case, that people who take these medications and exercise more, their heart rate doesn't go up as much when they're taking these medications. And while again, that seems like it would happen,

we are the first to provide definitive evidence of that. And that is really freaking cool, right? I mean, if it doesn't get cooler. Like often when you go into a study like this, like your hypotheses don't pan out. They fully did, like just as we would expect. And that's, that's awesome. Yeah, I love it. Research is hard. Painful. It's humbling. You know, you can do just, yeah, to your point, a lot of times we go in and we just, you know, you just don't see anything, you know, or what you expect to find isn't true, which is an insight in of itself. But to be able to come away with this analysis and, and, and, see the data that we saw was, I think, really, really special and such a great moment. And we do sometimes learn more when we don't see what we are. Right. But when it, when it does, it's like, wow, like you said, like, yeah. This is incredible. Like, and it's super cool. And I think it's super impactful for someone who's taking a GLP1 medication. And really what it's doing is

just supporting the recommendation, right? Exactly. It's been recommended that when you take these medications, you increase physical activity levels. And we're the first to provide evidence that that is a solid recommendation for cardiovascular health. As someone who has extensive expertise in sarcopenia and understands what's happening, a very mechanistic level, what would be your recommendation for folks who are on these drugs and maintaining quality muscle tissue, like just maybe walk through that? Because I think that's important. Yeah, and I think that's definitely where this research needs to go next.

Yeah, totally. You know, just this morning, we were talking. I was talking to my old postdoc advisor, you know, Roger Fielding, who the human nutrition research center on aging, the word sarcopenia came from there, right? It means poverty of flesh. And it came from the human nutrition research center on aging downtown. We were talking about GLP1 and his excitement for the research

and all of his colleagues talking about sarcopenia and GLP1s. And the reason why is very important, right? When people take these medications, we see that they're losing a lot of weight. 20% of their total weight is being lost in a year, but we see that almost half of that weight can come from muscle. And so the muscle loss with a year of these GLP1 medications is similar to that that we see with 10 years of human aging, right? Take these medications. You're losing a lot of weight, right? But that weight's coming from fat, and it's also coming

from muscle. That proportion varies how much of it's coming from muscle. And to be fully transparent, the implications of that for strength and performance and health span are not yet clear. But it still seems concerning, particularly if we think about the population who's taking these GLP1 medications, most of them are 40, 50, 60 years of age, which is right at the period where muscle loss is about to begin to accelerate. And so it seems as though throwing additional fuel on that fire is not something we would want to do. If you were to have to recommend, you know, so if someone's really limited time and they're choosing between doing cardiovascular work or musculoskeletal work and they're taking GLP1, what would you recommend they spend the most time doing? Yeah, I'm going to cheat on

that question and say both. I'm going to say a program that has them doing some sort of high intensity exercise, resistance training. To try to extenuate the effects of breast and heart rate and Yeah, but do resistance training, but then just take less rest between sets, right? Do something high intense. Do circuit. So maybe circuit training. Circuit training, exactly, which is lift heavy things. Characterized by like, you know, 45 second on, 15 second off, you know, just alternating muscle groups and adding some cardio. I did the circuit this morning, actually. There you go. Of course you know. But I think, you know, working, if you have the resources, getting a trainer alongside this journey, using Woop to kind of, you know, meet your strained heart. and, you know, calculate your musculoskeletal load. I mean, these things are all, you know, just inside our app ready for you to use as a resource to accompany you on whatever health journey you have, frankly.

But 100%. All right. Last question. So when you see the future of research at Woop, both kind of immediate and long term, without giving away any of our secrets, what gets you most excited? Yeah, no, great question. I think, you know, this paper really, you know, cross-functional paper and effort sets the table for the future of research at WOOP, right?

Which is to apply our learnings from some of the fittest human beings on Earth to make people live or help them to live longer and healthier lives. And how can we apply what we've learned from a study like this to, you know, to other conditions, right? Cardiometabolic disease, mental health, there are so many different ways that we could go with this. and using WOOP to unlock those secrets, I think, would be the best way to do it. Amazing. Well, Dr. Gisicki, thank you so much for your time today. I'm so grateful I get to work with you every day and learn from you. And I know our members are going to really, I think, love this conversation,

the insights that you provided today. Thank you, Kristen. It was a pleasure. If you enjoyed this episode of the WOOP podcast, please leave a rating or review. Check us out on social at Woop at Will Ahmed. If you have a question was to answer it on the podcast, email us, podcast to whoop.com. Call us 508-443-49-5-2. For anything about joining whoop, you can visit whoop.com. Sign up for a free 30-day trial membership. New members to use the code

Will W-I-L to get a $60 credit on Woop Accessories when you enter the code at checkout. That's a wrap, folks. Thank you all for listening. We'll catch you next week on the WOOP podcast. As always, stay healthy and stay in the green.