#319 ‒ Peter's key takeaways on liver health, heart rate variability, AI in medicine, klotho, and lactate metabolism ｜ Quarterly Podcast Summary #2
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Summary
In this episode of the Ask Me Anything (AMA) podcast, we look back at the interviews I did with Julia Wattacharro, Joel Jameson, Zach Kohani, Dina Dubal, and George Brooks. We discuss topics such as liver health, heart rate variability, AI and medicine, and Alzheimer s disease.
Transcript
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Hey everyone, welcome to a sneak peek, ask me anything or AMA episode of the drive podcast.
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I'm your host, Peter Atiyah. At the end of this short episode, I'll explain how you can access
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the AMA episodes in full, along with a ton of other membership benefits we've created,
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or you can learn more now by going to peteratiyahmd.com forward slash subscribe.
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So without further delay, here's today's sneak peek of the ask me anything episode.
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Welcome to another special AMA episode of the drive. Today's episode will be the second of
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what we're now calling the quarterly podcast summary. We did the first episode of this back
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in June and the feedback was overwhelmingly positive. In fact, I don't think we've ever
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received more feedback on the day of a podcast release than we did for the quarterly podcast
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summary number one. So it's no surprise that we're going to bring this back and continue to do it
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because again, people seem to really like this. And quite frankly, it's a lot of fun for me.
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These quarterly podcast summaries will look back at recent episodes released typically over the last
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quarter. And I'll discuss what I learned from the interview and what I think were some of the most
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important insights, as well as any changes in my behavior or thinking that resulted from the
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interview. In today's episode, we will cover the interviews that I did with Julia Wattacharro,
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Joel Jameson, Zach Kohani, Dina Dubal, and George Brooks. Throughout this, we speak on topics such as
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liver health, heart rate variability, the emergence of AI and its potential impact on medicine,
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the gene and protein clotho and its relationship to Alzheimer's disease and its
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potential to treat these conditions, and all things related to lactate. If you're a subscriber
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and would like to watch the full video of this podcast, you can find it on the show notes page.
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If you're not a subscriber, you can watch a sneak peek of the video on our YouTube page.
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So without further delay, I hope you enjoy this special quarterly podcast summary AMA of The Drive.
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Peter, welcome to another AMA. How are you doing?
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You're always welcome. So this will be the second episode that we've done like this,
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which is kind of our quarterly podcast summary. We released the first one back in June, received
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really positive feedback. People really liked it, wanted us to continue to do it. And so today,
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we're going to look at previous and recent episodes of The Drive. And as we look at them,
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we'll kind of look at what your key takeaways are from the episode, along with anything you changed
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as a result, whether behavior, whether your mind, whether how you're thinking about things,
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anything of that nature. And so today's episode, if all goes well, we'll cover topics such as the liver,
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liver health, heart rate variability and training, AI and medicine, clotho and Alzheimer's disease,
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lactate and more. So with all that said, anything you want to add before we get rolling?
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Only that I was so pleasantly surprised at how people took to the first episode of this quarterly
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summary that we did in June and said, Hey, that was the single most valuable piece of content you've
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ever put out. And what I thought was nice that there were people who said, look, these are episodes I
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didn't listen to. And now I just got the summary or these are episodes I didn't listen to. And I got
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this summary, which made me go back and listen to the actual episode or, Hey, I did listen to it,
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but honestly, it's just hard to remember everything. So I think when we sat here three
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months ago and recorded the first one, we were sort of like, well, you know, we hope people like it. And
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if you don't like it, we certainly won't waste anyone's time doing it. But I think it might be the
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most emails we've ever received for a single podcast with people saying this was fantastic. Please do
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it more. So it's really nice to hear that. And obviously it's our pleasure now to just make this a
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regular part of what we do each quarter. Yeah. And you kind of hinted at there too, is it's important
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to note these aren't replacements for listening to episodes. A lot of times they're good, either
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refreshers, good to figure out, to go back and listen to, or just to kind of put the pieces together
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based on what you heard. And so with that said, first episode we will look at is the one with
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Julia Wattachero on liver health, liver disease, NAFLD, MASLD, everything as it relates to the liver.
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So you want to kick us off? Yeah. This was an at times technical episode. This is a classic episode
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of the drive, meaning you don't expect to turn on a podcast and walk into a graduate level seminar on the
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liver. But if you take a step back and think about it, we kind of need to, right? It is arguably one
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of the most important organs in the body. It is certainly an organ as we discuss for which we have
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no extracorporeal support. Meaning if your kidneys fail, God forbid, that's very bad, but at least you
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have the option of dialysis. If your lungs fail, again, not a good thing, but at least you have a
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ventilator. Even if your heart temporarily fails, we have ways to support that outside the body.
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And yet remarkably, we don't have this for the liver. If a person goes into liver failure,
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their only solution is a liver transplant. And what that speaks to obviously is the diversity
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and complexity of function in this organ. So the role that it plays, and we really talked about
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it in three categories, metabolism, protein synthesis, and detoxification. There simply is
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no parallel for those things. Now we of course then talked about the role of alcohol. Everybody's
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aware, of course, that alcohol is metabolized by the liver and therefore that excess alcohol is
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toxic. But we talked a little bit about the how and the why, right? And that the metabolite of
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ethanol known as acetyl aldehyde basically causes all of the downstream problems by overwhelming the
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redox potential of cells in the liver. And that creates the attraction of free radicals and
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inflammatory cells. We did a great job, I think, really just talking about dose makes the poison here.
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So if a standard drink contains about 14 to 15 grams of ethanol, that will usually be found in
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about 12 ounces of a regular beer. Interestingly, my favorite beer, which contains like 10% alcohol,
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it would be, you'd get that 14 grams in far less. Five ounces of wine, one and a half ounces of liquor.
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So if you're trying to think about how much ethanol you consume, you have to be mindful of the drink.
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I noticed that when I'm pouring a glass of wine for myself or somebody else, it's never five ounces.
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It's probably closer to eight. So I don't think it's intuitive for people to think about how many
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grams of ethanol they're consuming. We didn't go much further into it here because we've done so
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much other content, which we can link to in the show notes about the toxicity of ethanol based on
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how many grams per day or grams per week you're consuming. Okay. Next major topic we got into
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was that of what is called MAZL-D or metabolic dysfunction associated steatotic liver disease.
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That's a mouthful. Why did we bring that up? Well, because you'll always hear me and for that matter,
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many other people talking about NAFLD or non-alcoholic fatty liver disease. So this was an
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education for me as well. And I think for the listener, which is we talk about NAFLD and that's been
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something that's been talked about for the last 20 years, it's the fastest growing form of liver
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disease in the developed world. And it's probably poised in its long-term sequelae to be the leading
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indication for liver transplant within the next decade. But the reason that the liver societies and
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the medical societies have taken on this name change is to basically be more encompassing.
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So again, NAFLD has the intuitive point of saying, okay, it's a fatty liver disease that does not
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result from the consumption of alcohol. Because of course, AFLD or alcoholic fatty liver disease
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would be the sort of sister disease. But this idea of MAZLD or metabolic dysfunction associated
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steatotic liver disease speaks to the complete overlap of insulin resistance, metabolic syndrome,
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type 2 diabetes here. Now, to be clear, the overlap is so strong that I honestly think for those of you
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as listeners, I don't know that it matters that much. According to Julia, 99.6% of people who meet
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criteria for NAFLD will also have the diagnosis of MAZLD. So at that level, it's not really clear.
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The diagnosis is based on metabolic dysfunction. So that's really the key thing when it comes to MAZLD
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is you also have to have insulin resistance, but it does not require fibrosis. It requires also that
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at least 5% of the hepatocytes, so hepatocytes are the liver cells, it's the functional unit of the
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liver, they have to contain fat. One of the things that we talked about that I used to know, and this
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is a great example of doing this podcast, is like there were things I once knew and then I kind of
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forgot. And this was one of them, was about the difference between kids and adults and the different
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pattern of fibrosis that they have. So in kids, it's more circulated around the portal vein.
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The portal vein, again, this is maybe a little more in the weeds than people want, but for me,
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it was very interesting. The portal vein is the vein that brings the majority of the nutrients
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to the liver. So the portal vein is formed by the confluence of two enormous veins in the abdomen,
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the superior mesenteric vein, and the splenic vein. And so they merge together and run into the liver,
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and that's carrying just tons of nutrients into the liver. And in that sense, the liver has two
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blood flows that are coming into it, one through the portal vein and one through the hepatic artery.
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So what's the implication of this? Well, the anatomy of it notwithstanding, what's the implication
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is what do you see from a diagnosis perspective? And in kids, you're going to see an earlier increase
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in ALT, AST, and GGT. Now, again, you'll often hear these things referred to as liver function
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tests. We talk about how we accept that as terminology, but the reality of it is they really
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tell us nothing about liver function. They are enzymes that are associated with liver or hepatocyte
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health. And when those enzymes go up, we generally understand that some sort of injury has taken
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place. We'll talk about that more in a moment. In adults, the fibrosis and steatosis tends to occur
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closer to the central vein. And as a result of that, you see a delay in the enzyme elevation.
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So what does that mean clinically? It means that if you're an adult and you're developing steatosis
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and fibrosis, it could actually be taking place for quite a while before you see it. And that's
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why another huge takeaway, which I'll get to in more detail in a moment, is that this reliance
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on elevations of the transaminases, which are the technical names for ALT and AST, and using that as
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your threshold for concern might be waiting a little bit too long. Okay. So now if you look at the
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top three causes of liver injury in the form of steatosis and fibrosis, you have Masaldi number
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one, followed by alcoholic liver disease, again, something we should never forget. And then finally,
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infections of which hepatitis is the most common. And real quick on that, Peter, just so people
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understand is we had an older episode with Chris Sonnende on organ transplantation. And back in that
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episode, you all talked about the liver, but the fact that Masaldi is now number one is something
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that wasn't even close to true 20, 30, 40 years ago, correct? Yes. In fact, I even write about this
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a little bit and outlive that I recount a story when I got either a medical student or an intern
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more than 20 years ago, operating on a patient. And one of the jobs, I think it was when I was an intern,
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because one of the jobs of the intern is to pre-op the patient. Pre-op the patient means get them
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ready for surgery. And among those things is understanding how much alcohol they consume.
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Because when a patient is undergoing major abdominal surgery, as was this patient for the
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resection of a colon cancer, alcohol withdrawal, it's a very serious medical complication. So
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patients who are drinking three or four drinks a day when they're in the hospital will either need
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to have a continuous infusion of ethanol, or they'll have to have more benzodiazepines to cope with
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the withdrawal, which can actually be fatal. So point of it is, you better understand how much alcohol
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your patient drinks. And I'm talking to this guy the night before surgery, and he's telling me he
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doesn't drink anything. Okay, great. Whatever. I ask you in a de-arming way. It's not like,
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these are questions that people typically answer without reservation. We get into the operating room
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to do surgery on this guy, and his liver looks like it's a piece of fat. And at the time, I think
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everybody just assumed, A, I was a moron for not finding this out ahead of time. And B, once they
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realized, yes, I did in fact ask that he was lying. And in fact, what I now realize, because we never
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really gave it another thought, I wish I could tell you like this led to some lifetime journey
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of mine to understand it. It was just, all right, let's get his colon out and make sure his cancer's
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gone. But I now look back and realize this guy clearly had what we would have at the time called
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NAFLD. So that's a long-winded way of saying you're absolutely right. 20 to 25 years ago, this was
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really not something that was recognized, although it was probably far more prevalent than we believed.
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But I would say that by, I would say 2010 to 2012, most people felt like this is an epidemic,
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and this is going to be an enormous burden on the healthcare system as far as liver transplantation.
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Again, getting back to the point at the outset, which is that extracorporeal support of a dysfunctional
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liver is not possible. So we should spend just a second talking about hep B and hep C.
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Obviously, people have heard of those things. For hep B, we do have a vaccine today. For hep C,
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we do not. Conversely, for hep C, we have a treatment, whereas for hep B, we do not.
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So the net-net is if you're someone who's coming of age today, you're a teenager today,
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you're probably going to have a hep B vaccination, which is going to protect you from that. And should
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you contract hep C, you're going to have a treatment. However, there are many people for whom
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hep B was acquired before a vaccination was prevalent. And why do we care about this? Well,
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we care about it for two reasons primarily. The first is the risk of liver failure and all of the
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things we talk about through this pathway of steatosis, fibrosis, and ultimately what is called
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cirrhosis, the irreversible fibrotic change of the liver. But the other thing we have to talk about
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here is hepatocellular carcinoma, which is a deadly type of cancer if not caught very, very early. And
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so the cancer risk here is a greater issue from the infectious side. So you always want to be
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screening patients for hep C and hep B regardless of the workup. So in other words, when we're working
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patients up for usually the first thing we're seeing is this elevation in transaminases, we're
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also including a hep C and a hep B workup. The other thing to keep in mind here is that
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Masal-D and alcoholic liver disease are also increasing the risk of hepatocellular carcinoma.
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So it's not just hep B and hep C. And as a general rule, again, this was something I learned in the
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podcast, either I'd forgotten it or never knew it, that as the scarring and fibrosis of any of these
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diseases, Masal-D, alcoholic liver disease, hep C, hep B, as the degree of scarring and fibrosis,
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increases, so too does the risk of cancer. And by the way, I misspoke there a little bit.
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For hep B, that risk is regardless of disease progression. So let me just restate that. So
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hep B, you're going to see about a 3% to 5% per year cancer risk, regardless of where you are in
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the disease. So fortunately, again, we have a vaccine to reduce your risk of that. But for the others,
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the risk of cancer goes up with the risk of disease. Okay. I think the last thing to talk about on this
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topic is how do you make the diagnosis? Because the gold standard for this is to do a biopsy.
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And it's not that a liver biopsy is as complicated as a cardiac biopsy or even a lung biopsy, but
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that's not a procedure you would just go and do willy-nilly to stick a needle into the liver
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with its risk of bleeding primarily or also infection. So really what we want to do is understand
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how to make this diagnosis non-invasively. So look, again, nobody wants to do a liver biopsy.
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So we're really talking about blood-based biomarkers and radiographic or imaging modalities.
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Let's start with the blood-based biomarkers. If we're now going to look at blood-based biomarkers,
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the two most common of these, the transaminases, which again are erroneously and often referred
00:17:02.760
to as liver function tests, are ALT and AST. And unfortunately, we cannot diagnose MASLD
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slash NAFLD with those biomarkers. Now, the reason that we see an elevation of these during
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fat accumulation and or fibrosis in the liver is that these are enzymes made by the hepatocytes
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that are released into plasma when the liver is stressed. So as you see more ALT and AST,
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that indicates more stress. But it gets a little complicated because AST is also found in muscle.
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And therefore, as you exercise, you will also see more AST increased into the plasma. And in fact,
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that's one of the things we use to try to understand this. My AST is always higher than my ALT.
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My ALT is typically in the mid to high 20s. And my AST is typically in the low to mid 30s. That is the
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typical pattern for me and for many of our patients. And we know that that is a pattern that is pretty
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typical of people who are doing quite a bit of exercise. The general rule of thumb is that you
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would like to see an AST and ALT both below about 30 IU per liter. Again, I just told you that my AST
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is typically a little bit above that. Normal results for me might be an ALT of 25 or 26 and an AST of
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33 or 34. Am I concerned about that? No. I've obviously, being a curious person, done some more
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imaging stuff to make sure there's nothing going on. But ultimately, you just have to handle each of
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these situations kind of clinically. There are also pharmacologic things that will raise them. So
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lipid lowering drugs are a very common offender and will raise AST and ALT. What is the threshold
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at which you should be concerned? If you typically see somewhere between a one and a half and twofold
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persistent increase, that would really justify investigation. Even if it's in response to a
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drug, it would probably justify stopping that drug. For example, if you're on a statin and this is
00:19:09.660
happening, that's probably reason to stop a statin. And certainly in our practice, it is, even though the
00:19:14.320
guidelines might suggest you tolerate a higher level of increase. When you kind of say stop a
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statin, does that mean if you're treating someone with a statin for potential CBD risk and you see
00:19:26.100
the liver enzymes increase, you abandon treatment or are you just looking at potential other drugs to
00:19:32.780
handle the CBD? Yeah, it would be the latter. So in other words, we treat the CBD or ASCVD risk
00:19:38.960
using the tools that are available. But I'm just saying that we include elevations of transaminases
00:19:45.780
in the suite of things that we would view as a contraindication. So look, I don't think any doctor
00:19:51.640
out there would say, I'm going to give my patient a statin, but if they develop debilitating muscle
00:19:56.320
pain, we're just going to keep hammering them with it. Of course not. Four to five percent of patients
00:20:00.480
will develop significant myopathy from a statin use. It's reversible, but obviously you're going to
00:20:06.240
stop the drug and find an alternative. We would just consider a significant elevation in transaminases,
00:20:12.300
a change in insulin sensitivity. Those would be the big three things we always look to
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get people off a statin or at least off one statin onto another or just off the class altogether.
00:20:21.900
Let's talk about what maybe is a better test here because I sort of just alluded to the fact that
00:20:26.640
those tests don't work very well. They really lack sensitivity and specificity. So if a physician
00:20:33.900
really wants to understand if their patient has Mazel-D and make that diagnosis, they really want
00:20:40.160
to understand how much fat is present and how much fibrosis, if any, is present. And my takeaway was
00:20:46.140
that the gold standard was probably magnetic resonance elastography and proton density fat
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fraction or PDFF. So that's sort of looking at MR technology, so meaning an MRI to make the diagnosis.
00:21:00.000
Now, the problem with this is that it's obviously costly and it's not a widely available test.
00:21:06.320
You can't just go to an MRI and get that done. That's a very specific protocol. So I would say from
00:21:12.140
a practical standpoint, the more common tool are ultrasound and vibration methods that are less
00:21:19.400
expensive, that are easier to do in a clinic. And there's a branded version of this that we typically
00:21:25.660
use called fibroscan. So it's a vibration controlled transient elastography, and it uses both vibration
00:21:33.360
and ultrasound to basically give what's called a cap score. Again, I don't know that the details of this
00:21:39.760
are entirely needed. For us, it's interesting because we do these things, but basically this cap score is
00:21:45.260
called controlled attenuation parameter. And we actually want to see that number. So now we're
00:21:51.960
actually able to quantify the degree of fat and fibrosis in the liver. And now we have a biomarker
00:21:58.860
that we're treating. Because remember, although we didn't talk about it enormously in this podcast,
00:22:03.500
because we've talked about it so much elsewhere, the real question here is what are we doing when
00:22:07.640
we have this information? So you've now confirmed your patient or you as the individual have fat or
00:22:12.140
fibrosis in your liver. Now what? Well, here's the thing. It's not a really clear indication for a
00:22:18.040
drug per se. This is something that is going to respond most favorably to a reduction in excess
00:22:24.280
adipose tissue and an improvement in insulin sensitivity. And of course, depending on the
00:22:27.920
etiology or removal of the insulting agent. So, you know, I guess the way I would close this summary up
00:22:33.720
would be to say that what are we doing when we see this? Well, we're getting our patients to lose
00:22:39.220
weight. And again, that's not an easy thing to do. It is simple, but not easy, right? Simple in concept
00:22:44.740
can be challenging in practice, although at times it relies on drugs like GLP-1 agonists,
00:22:50.360
but we're also being mindful of taking things away. So if a patient, let's say, is drinking
00:22:56.000
five or six drinks a week, which would not be considered excessive, but their FibroScan score
00:23:01.640
comes back showing modest steatosis and or fibrosis, well, we're going to take all alcohol out of their
00:23:07.100
diet. Because why would you add any additional insults? So in addition to putting them on a program
00:23:12.780
that's going to help them lose weight and improve insulin sensitivity, we're going to remove alcohol.
00:23:18.100
The other things we're going to do, although I think we have far less data for this, are going to be
00:23:22.620
remove liquid fructose from their diet. So every time a study has been attempted, to my knowledge,
00:23:29.420
to look at the isocaloric impact of liquid fructose, it has been unable to discern if that is different
00:23:37.580
from isocaloric glucose because the subjects usually end up losing weight, even when you make an
00:23:42.300
attempted isocaloric substitution for fructose to glucose in liquid form. So in other words, two things
00:23:47.440
change and you can't tell. That said, we continue to abide by the idea that liquid fructose and
00:23:53.340
alcohol should probably be minimized if not avoided in people with mazaldi slash nafaldi. So it's a bit
00:24:00.120
of a long summary, but it is a very important topic. And I hope that either for folks who have listened
00:24:05.360
to it or plan to go back to listening to it, this can sort of prime that discussion.
00:24:10.140
One follow-up question on what you said. If someone is kind of curious on the state of their liver,
00:24:16.760
you mentioned ultrasound might be the easiest and most widely available thing. Do you have all your
00:24:22.580
patients get ultrasounds to test their liver or is it only if you see potentially other things that
00:24:28.260
are concerning that you want to see the state of it?
00:24:30.400
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