Welcome back, team, to the Building Lifelong Athletes podcast. Thanks so much for stopping by. I really appreciate it. If we haven't had a chance to meet it, my name is Jordan Renke, and I'm a dual board certified physician in family and sports medicine. And the goal of this podcast is to give you active penalty for life through actual evidence-in-form education. Today, we're talking all about coffee atrial fibrillation and a recent trial that came out. This podcast is going to be a little different. I'm trying a couple things here, shifting a little bit. So, essentially, what I've done now is I've made a shorter YouTube video. I've just found that on YouTube, people don't really care about long form videos. Going into the 30, 40 minutes sometimes for podcasts, people don't really seem to care about that. And it just doesn't seem to be Yeah, hitting that right audience there. So, what I'm gonna do is make shorter videos on YouTube and shorter to the point, you know, anywhere from Five to probably 20-ish minutes, depends on how nerdy I'm going to get and deep in there. And I'm going to have that video, and essentially, that's going to be my video podcast. It's during your video, so I will still have it on YouTube. It'll still be on the YouTube playlist for podcasts, all that stuff. But I'm going to do a little deeper or more context here in the audio podcast itself. So, what we'll do is we'll play that video today. And then at the end of that video, we are going to kind of go a little more in-depth, just adding a little more nuance to it, just because the The video, I just find that in retention-wise, people just don't care about nuance on the video platform. And whereas the podcast, that's kind of what people expect, right? They sign up for a little more nuance. And then we're nerdiest. And so that's what it's going to do. We're going to go watch the video, get the highlights, and then we'll go a little bit further, just talk about a couple of things that are kind of important. And then That'll be it. So, hope you enjoy this new format. Let me know if you think it's the dumbest thing in the world, but I appreciate any feedback you have on it. There is arguably no piece of advice more common for people with heart rhythm issues than this: cut the caffeine. Whether you have the occasional palpitation or you've been diagnosed with atrial fibrillation or just worried about your heart health, the conventional wisdom has always been that coffee is enemy number one. And it makes sense, right? Caffeine is a stimulant, AFib is an irregular heart rhythm. Why would you pour fuel on the fire? But here's the thing: what if that advice is actually wrong? What if stopping your daily coffee habit isn't just unnecessary suffering, but actually making your heart less stable? A brand new randomized controlled trial called the Decaf Trial, wonderful name by the way, just challenges dogma in a massive way. And the results were pretty striking. We're talking about a 39% lower risk of AFib recurrence in the people who kept drinking their morning coffee compared to those who quit. So, today we're going to go through and separate the internet lore from the medical reality. We're going to break down this exact study: what was done, why a stimulant might actually be protective for the heart. And whether you actually need to change your morning routine. Let's dive in. So, first and foremost, we have to address the elephant in the room, which is the conventional wisdom, right? So, for decades, doctors, including myself, Have often operated on the assumption that caffeinated coffee is pro-arhythmic, meaning it causes abnormal heart rhythms in your heart. It increases sympathetic tone. It can raise your blood pressure, and patients often report that they feel like it triggers them. And so, because of that, the standard of care is often meant to play it safe and tell people to abstain from caffeine. But because I'm a nerd, I wanted to look through the data. And for years, the large-scale observational studies have shown this weird protective signal, right? Time and time again, we see that habitual coffee drinkers don't actually have high rates of AFib. They often have lower rates. But we couldn't necessarily trust that, right? We thought maybe there's a healthy user bias. Maybe people who drink coffee just exercise more, or maybe the people who get palpitations naturally stop drinking coffee. So the ones left drinking are the ones with iron hearts, who pretty much can do anything to them and it won't matter. So, we needed a real experiment to know for sure. And so, we needed a randomized controlled trial. And that's exactly what the decaf trial gave us. So, let's take a step back and look at how they set this up because the design is crucial, right? They took 200 patients who were habitual coffee drinkers, meaning they normally had coffee. And here's the important nuance here: these weren't just random people, right? They had atrial fibrillation or atrial flutter, so they had to have that. And they were scheduled for an electrical cardioversion. All this means that their hearts were out of rhythm, right? And the plan was for them to go to the hospital and get their heart shocked back into a normal rhythm. And with these people, this is a high-stakes population. We know that recurrence rates are pretty high. We can have a sometimes 50% recurrence or going back to that abnormal rhythm within six months. So, if coffee was going to be a trigger, This is the group where we would see it. Once these patients were successfully shocked back into their normal rhythm, they were randomized into two groups. First, we had the consumption group. These folks were told to keep drinking their caffeinated coffee, aiming at about one cup per day at least. Then we had the absence group. These folks were told to stop completely: no coffee, no caffeine. And then they watched both these groups for six months to see whose AFib came back. And so, what happened? Well, if you follow the old school advice, you'd expect the coffee drinkers to be jittery and their hearts to go back into a faster. But the data showed the exact opposite, actually. In the abstinence group, the people who quit. 64% had a recurrence of the rhythmia, but in the coffee consumption group, only 47% had a recurrence. And when you crunch the numbers, that is a hazard ratio of 0. 61. And you might be like, Jordan, what does that mean in real life? Well, that's a 39% low risk of having your AFib come back just by continuing to drink your coffee. Now, let's take a look at this chart right here. This is something called a Kaplan-Meyer curve, which shows the probability of an event over time. A lot of times, this is used to look at mortality, but we can look at it for a bunch of different things. On the y-axis, we have the probability of recurrence, meaning the probability of your AFib or atrial flutter coming back. And on the x-axis, you have the days of follow-up. So, how long we have follow-up there. You can see the line separate almost immediately. So, this means that the people drinking coffee stayed in normal rhythm longer and more often than the people who quit. And you can see this divergence, and this divergence really kind of shows us that, hey. There's a real signal going on here. It's not just kind of, oh, maybe it's happening, but no, they're showing that, hey, definitively, we see these people who continue to drink coffee had better outcomes long term. And so, this kind of brings up the obvious question: why is this happening? How on earth is a stimulant protective against something like AFib? It seems counterintuitive, but there are a few possible plausible mechanisms we're going to talk about. The first proposed mechanism has to do with something called adenosine. And we know that caffeine blocks adenosine receptors in the body. And adenosine is a chemical that in the heart can actually shorten something called the refractory period of the atrium. So, refractory period just means how long does it take until your heart is ready to pump again? And adenosine in the heart muscle, it makes it ready to fire too quickly, which could potentially facilitate AFib. So, by blocking these adenosine receptors, caffeine might actually be preventing the heart. From being too twitchy. The second mechanism is inflammation. And we blame pretty much everything on inflammation, and this is no different. But coffee is packed with biological compounds that have known anti-inflammatory properties. So, the idea is that because we know that inflammation could drive AFib, these chronic anti-inflammatory effects of coffee may be helping stabilize the heart some way. And finally, there's the behavioral factor. The researchers pointed to a previous study called the Crave Trial, which showed that people who drink coffee tend to have about a thousand more steps per day than non-coffee drinkers. And physical activity is one of the best drugs we currently have for preventing AFib. So it's possible that coffee gives these patients just enough energy to be a little more active. Which is actually protecting their hearts. But, and there's always a but, we have to apply some nuance here, right? I don't want you to hear this and think that coffee is just a magic cure-all, There were definitely some limitations we need to talk about. The first limitation is selection bias. So, in this study, they screened nearly 2,000 people just to find 200 people who were willing to participate. A huge chunk of these people were excluded because they refused to quit coffee. Essentially, they just said, no, it's not worth it. I love my coffee. I'm not going to do that. Or the other reason, and this is key, is that they refused to drink it because they knew that it triggered them. So they're saying, hey, if I drink this, I'm going to go back into AFib or it's going to give me palpitation. So they excluded all those people. And so if you're someone who drinks a cup of coffee and immediately goes into AFib or hurt them, please listen to your body. Do not listen to me. I'm just a random dude on the internet. Please do not do that. You're definitely an N of one, and this research experiment does not talk about you, right? It does not apply to you. So, do not force yourself to drink it just because a study said so. This study looked at people who were already proven to be coffee tolerant. Second, this was a study on continuation, not initiation, right? So these patients were already coffee drinkers. We aren't telling people who hate coffee to start chugging espresso for heart health. That's not what I'm saying. And lastly, we're also talking about coffee specifically, not energy drinks or caffeine pills. Coffee has a complex matrix of antioxidants and different compounds that you don't get in sugar energy drinks. So we can't just extrapolate this to any sort of caffeine. So, what does this actually mean for you? Well, here are the takeaways. If you have AFib and you enjoy your morning coffee and you don't feel like it triggers symptoms, you likely don't need to stop. In fact, the stress of withdrawal and the loss in your daily ritual might be worse for your heart than the caffeine itself. And we really want to focus on the big rocks, right? So we talk about sleep, diet, alcohol cessation, exercise, weight management, all those big things. These move the needle. Demonizing a bean that brings you joy, that's probably not worth the energy. As always, I'm just some dude on the internet. So make sure you talk about this with your doctor if you do have AFib or are concerned about this. But hopefully, this makes you feel a little more confident that your daily coffee isn't ruining your heart. All right, so hopefully you enjoyed that. That was the YouTube video of it. Now, here, one thing I want to talk about specifically was what kind of triggered this decaf trial, right? So we had the Crave trial first. This is. Early on. So, before testing the long-term therapeutic effect of coffee in a disease population, meaning this decaf trial, this same research group actually did this decaf Led by Dr. Marcus's name, they had to answer a more fundamental question, right, in a healthy population. And that was if coffee led to real-time atrial or ventricular ectopy. So, these additional beats in the atria or the ventricle, that's what's going on. And so, the CRAVE trial was created. It was actually really important, right? Because it kind of set the tone for it. It employed a different design. It was a randomized N of one case crossover trial. And it had a different population, so a hundred healthy adults. And so, to answer the question, they asked, what are the acute or day-to-day effects? Of coffee consumption on arrhythmia precursors, right? So we kind of think: hey, these beats, these potential actabe beats, these atrial matricular actabe. These could be precursors to arrhythmias. And so, hey, what happens when we consume coffee in healthy people? Does it lead to additional things? And so, the key findings were about three main things. First, there was no increase in atrial activities or PACs, so premature atrial contractions, or that's what we look at. The primary outcome was daily premature atrial contractions, which are a known trigger to atrial fibrillation. So, super common to see this all the time. These PICs, if the burden is pretty high, can lead to having palpitations. And so that's what we looked at. The trial found no significant difference in the number of daily PICs on days participants consumed coffee versus the day they abstained from that. Finding cited by the decaf authors was a critical safety signal, right? It provided the first RC2 level evidence that acute coffee consumption was not a significant trigger for the precursors for atrial fibrillation. On top of that, they looked at ventricular ectopy as well. So the trial did find in this early trial, did find that coffee consumption was associated with. Significantly more daily premature ventricular contractions. So, PVCs. So, we have PACs, now PVCs, they did say that. So, this suggests that atrial and ventricular tissue may respond differently to caffeine. So, we did not see the PACs, but we did see PBCs. And we think about atrial fibrillation, so atrial fibrillation, right? It's going on the atria. So that's why we say, okay, in the atria, didn't really see it happening in ventricles. Maybe we did, but maybe that's not important for. AFib because it's not in the atria itself. So that's what they talked about. And on top of that, the third main finding that they found here was really cool. They found that coffee consumption was associated with more physical activity and less sleep per day. Interestingly enough, they found that the people did about a thousand more steps per day who are consuming caffeine and slept 36 fewer minutes per night. And so, just kind of cool, interesting findings. And I mentioned that in the video as well, that could play into a role that, hey, these people are actually being more physically active, and physical activity is wonderful for AFib. So, maybe that's what's going on. And so. Those are the things that they mentioned here. And it was a nice foundation for this decaf trial. You know, this goes back, it's kind of nerdy. It's not as critical to understand for the decaf trial, but it helps lay the groundwork, right? It demonstrated that in healthy individuals. Coffee was safe from atrial ectopy, at least that standpoint, providing the mechanistic plausibility and ethical grounding to proceed with a longer-term bigger trial in people with disease population, right? So people who have atrial fibrillation or flutter. And kind of, yeah, it also laid the groundwork for other models for why that could be happening or why AFib and caffeine could or could not be linked. So I thought it was kind of cool. Precursor to the study and worth mentioning. And some additional details for the actual decaf study now, right? So we talked about primary objective. Primary objectives were to assess the effect of abstaining from coffee compared to a continuation of coffee. On the first recurrence of atrial fibrillation or flutter, analyzes a time-to-event outcome. And the primary endpoint was defined as the first confirmed clinical recurrence of AFib or flutter. Or a device-detective occurrence lasting longer than 30 seconds following this cardioversion. So they all got cardioverted first, and then we kind of looked for it. The hypothesis was pretty much that, hey, if you stop, you know, the generic idea was that, hey, if you don't consume caffeine, you're going to have A better time and better outcomes. And obviously, that's what we look for. We did talk about study design and protocol there. The big thing that was worth mentioning was that for detecting these events. And they pretty much had a pretty it was pretty random. They were like, okay, on EKG or like your own personal, like, probably like Apple Watch or whatnot. So that was definitely a huge limitation of that. And I thought worth mentioning that it was like. There's no real set way that they were determining that. So I thought that was kind of interesting. But either way, it was done all over. It was done in the US, Canada, and Australia as well, which was great. And then the randomization, as I mentioned, only 200, it took forever. To get there. And they initially had intended on following up for 12 months, but to facilitate recruitment, and given frequent reluctance of patients to abstain from coffee, they turned it to six months' duration. So, once again, I found that to be like the funniest thing that people were pretty much like, oh, stop coffee for six months to a year. Yeah, no, I'm out. Like, I'm out. And obviously, that just shows the importance of coffee for a lot of people, not only just from a Social and cultural perspective, but yeah, it's just people aren't going to do that. And so that was, I thought, really interesting. It's worth worth mentioning as well: inclusion criteria had to be at least 21, although they were significantly older than that. In the mean age, it was about 69%, and 70% were male. And they did have a high prevalence of comorbidities, including 64% hypertension, sleep apnea, 28%, and heart failure, actually at 22%. And that's kind of the big things. And as I mentioned before, We're not going to re-go through the study with findings, what they found, but once again, it was kind of interesting to see that when these people Consumed coffees seem to have less recurrence of their AFib. It's still almost 50%. I mean, let's be honest. It's not great. It's 64 to 47. So it's not like, oh, it magically heals people. But it was cool to see that, hey, mechanistically, caffeine might not be the thing you have to throw at, which I thought was kind of cool. For secondary endpoints, I think worth mentioning as well, there was a comparable benefit that was observed when analyzing the atrial fibrillation recurrence only, excluding atrial future, which meant also met statistical significance. Um, yeah, so maybe once again, they looked just at AFib. They said, Yep, so what they're saying here is it's not just you know the atrial flutters can confounding it, it's in and of itself, AFib also seemed as well. So, that's kind of what it is. Other things that I do want to talk about, some methodological strength and limitations. As I mentioned, this is an RCT, which is wonderful. This is really the first one of that. That's really paramount to why we think this is so strong. And I think I applaud them. Obviously, there's limitations, but that's great. We need that. We found a significant finding and an overall generalizable design for the intervention. Either you do coffee or you don't. So I thought, oh, kind of cool. A couple limitations, though, I did want to mention that I didn't mention in the video is that the open label design. So, this is the trial's most significant weakness, I think. Both patients and investigators were aware. of the treatment allocation, right? So this can induce performance and detection bias, meaning patient in the abstinent groups is a little more anxious about triggers. Or report symptoms more readily. And the authors argue this is mitigated because the endpoint was detected and confirmed by treating physicians and not the study staff, making it more objective. But overall, still, it's open label, they know what's going on, which is going to be hard. I guess you could do caffeinated versus non-caffeinated and randomize people to that. But then, what are you like delivering coffee to them every single day? That's not a practical design. Oh, that'd be pretty sick. You should do that if you're out there and you want to. I do a study, that'd be cool, and then also a sample size of 200. I'm not huge, definitely adequately powered for its primary endpoint. But this is a modest sample size and leaves a chance that you know that hey, maybe this is just a chance finding. Once again, hard to recruit people here. It sounded like they went through 2,000 people and only ended up with 200. So that's what they're going for. And yeah, and that's what it is. And then, as I mentioned, the pragmatic endpoint detection limitation is the trial did not employ a standardized protocol mandated. detection method for all patients, which I thought was kind of crazy. You know, like that's like the big limitation. Use like a 30-day monitor at six months to see if they've gone back into it. Instead, they relied on Clinically detected atrial fibrillation from a variety of sources: 12 EDKG, consumer devices, implanted devices. Yeah, but There was a data table in there that did mention that the coffee consumption group used more wearable ECG monitors, 21%, than the abstinence group, which was 0%. And this difference differential surveillance could potentially increase the detection of atrial fibrillation in the coffee group, biasing the results towards the null. And so they're saying, hey, actually. People who we thought would find it more didn't. And so, is that either way, who knows what's going on? Um, I thought they were worth mentioning, and that's kind of where it comes. And so Yeah, this is kind of cool, right? So we've kind of walked through this coffee where, you know, first of all, it's clinical lore, right? Like, oh, like conventional wisdom, don't have coffee. Coffee is bad for you, it makes your heart You know, leads to AFib or different rhythmians, whatnot, that seems to be refuted by this data, saying, hey, that's not the case. But I will obviously be clear. Everyone is different. This is a study, right? A study indicates a bunch of people and not an individualized person. So, if you, as an individual person, say, hey, actually, I get this, this is what happens. And well, then obviously. You're not the study. But overall, in this study, we didn't see that noise. You know, the observational data that did say, hey, we don't see the link between caffeine and AFib or arrhythmias, that is confirmed. It seems to be supported by this evidence. And then it's kind of cool with this RCT here, right? And then you have the Crave trial and then the DCAF, both showing, hey. Mechanistically, caffeine doesn't seem to lead to arrhythmias, or at least to atrial arrhythmias. Obviously, going back to that early kind of crave findings that, hey, maybe you have PBCs, but doesn't seem to lead to TACs. And so, yeah, I think that's kind of interesting. At least worth thinking about. You know, as a doctor, I've seen this all the time: like, hey, stop coffee. And I still like, I probably would recommend people: like, hey, if you're getting triggers, let's try without it. And if they say, Hey, I noticed no difference, then you can kind of stay on it. It makes me feel a little better to give recommendations that, hey, maybe we don't necessarily need to do this. But yeah, that's going to be it. Hopefully, you found this helpful. Hopefully, this format here for me is helpful to do, if I'm being honest with you, just in terms of focusing on doing the video and then explaining a little deeper. A lot of people don't really care. And podcasts are just a little nicer for free-flowing conversations and have more time, usually, for people. You know, most people want to look, don't want to look at my ugly mug for 30 minutes on YouTube, whereas on a podcast, you're stuck in the car with me. So, but if you feel strongly that this is a terrible decision, please let me know. But otherwise, I'll probably do this for a little bit to see how that goes and how the workflow goes. Um, but I appreciate either way if you are listening, that doesn't mean the world to me. Like, seriously, there's so many podcasts in this world, and if you're listening to my voice right now, yeah, that really means a lot to me. But That is going to be it for today. Now get off your phone and get outside. Have a grass of your day. We'll see you next time. Disclaimer, this podcast is for entertainment, education, and informational purposes only. The topics discussed should not solely be used to diagnose, treat, or prevent any condition. The information presented here was created with an evidence-based approach, but please keep in mind that science is always changing, and at the time of listening to this, there may be some new data that makes this information incomplete or inaccurate. Always seek the advice of your personal physician or qualified healthcare provider for questions regarding any medical condition.
