The Peter Attia Drive - #319 ‒ Peter's key takeaways on liver health, heart rate variability, AI in medicine, klotho, and lactate metabolism ｜ Quarterly Podcast Summary #2

00:00:00.000 Hey everyone, welcome to a sneak peek, ask me anything or AMA episode of the drive podcast.

00:00:15.820 I'm your host, Peter Atiyah. At the end of this short episode, I'll explain how you can access

00:00:20.280 the AMA episodes in full, along with a ton of other membership benefits we've created,

00:00:24.900 or you can learn more now by going to peteratiyahmd.com forward slash subscribe.

00:00:30.600 So without further delay, here's today's sneak peek of the ask me anything episode.

00:00:38.920 Welcome to another special AMA episode of the drive. Today's episode will be the second of

00:00:45.060 what we're now calling the quarterly podcast summary. We did the first episode of this back

00:00:50.120 in June and the feedback was overwhelmingly positive. In fact, I don't think we've ever

00:00:55.140 received more feedback on the day of a podcast release than we did for the quarterly podcast

00:01:00.560 summary number one. So it's no surprise that we're going to bring this back and continue to do it

00:01:05.740 because again, people seem to really like this. And quite frankly, it's a lot of fun for me.

00:01:10.620 These quarterly podcast summaries will look back at recent episodes released typically over the last

00:01:15.400 quarter. And I'll discuss what I learned from the interview and what I think were some of the most

00:01:19.740 important insights, as well as any changes in my behavior or thinking that resulted from the

00:01:25.320 interview. In today's episode, we will cover the interviews that I did with Julia Wattacharro,

00:01:29.880 Joel Jameson, Zach Kohani, Dina Dubal, and George Brooks. Throughout this, we speak on topics such as

00:01:37.360 liver health, heart rate variability, the emergence of AI and its potential impact on medicine,

00:01:43.440 the gene and protein clotho and its relationship to Alzheimer's disease and its

00:01:49.240 potential to treat these conditions, and all things related to lactate. If you're a subscriber

00:01:56.480 and would like to watch the full video of this podcast, you can find it on the show notes page.

00:02:01.700 If you're not a subscriber, you can watch a sneak peek of the video on our YouTube page.

00:02:06.480 So without further delay, I hope you enjoy this special quarterly podcast summary AMA of The Drive.

00:02:12.420 Peter, welcome to another AMA. How are you doing?

00:02:21.020 Good. Thanks for having me back.

00:02:23.080 You're always welcome. So this will be the second episode that we've done like this,

00:02:29.540 which is kind of our quarterly podcast summary. We released the first one back in June, received

00:02:34.800 really positive feedback. People really liked it, wanted us to continue to do it. And so today,

00:02:40.500 we're going to look at previous and recent episodes of The Drive. And as we look at them,

00:02:46.840 we'll kind of look at what your key takeaways are from the episode, along with anything you changed

00:02:52.600 as a result, whether behavior, whether your mind, whether how you're thinking about things,

00:02:57.820 anything of that nature. And so today's episode, if all goes well, we'll cover topics such as the liver,

00:03:03.600 liver health, heart rate variability and training, AI and medicine, clotho and Alzheimer's disease,

00:03:09.780 lactate and more. So with all that said, anything you want to add before we get rolling?

00:03:16.620 Only that I was so pleasantly surprised at how people took to the first episode of this quarterly

00:03:22.400 summary that we did in June and said, Hey, that was the single most valuable piece of content you've

00:03:28.440 ever put out. And what I thought was nice that there were people who said, look, these are episodes I

00:03:33.560 didn't listen to. And now I just got the summary or these are episodes I didn't listen to. And I got

00:03:40.060 this summary, which made me go back and listen to the actual episode or, Hey, I did listen to it,

00:03:44.300 but honestly, it's just hard to remember everything. So I think when we sat here three

00:03:48.300 months ago and recorded the first one, we were sort of like, well, you know, we hope people like it. And

00:03:52.060 if you don't like it, we certainly won't waste anyone's time doing it. But I think it might be the

00:03:56.040 most emails we've ever received for a single podcast with people saying this was fantastic. Please do

00:04:01.880 it more. So it's really nice to hear that. And obviously it's our pleasure now to just make this a

00:04:06.760 regular part of what we do each quarter. Yeah. And you kind of hinted at there too, is it's important

00:04:12.060 to note these aren't replacements for listening to episodes. A lot of times they're good, either

00:04:16.760 refreshers, good to figure out, to go back and listen to, or just to kind of put the pieces together

00:04:23.140 based on what you heard. And so with that said, first episode we will look at is the one with

00:04:29.380 Julia Wattachero on liver health, liver disease, NAFLD, MASLD, everything as it relates to the liver.

00:04:37.380 So you want to kick us off? Yeah. This was an at times technical episode. This is a classic episode

00:04:43.940 of the drive, meaning you don't expect to turn on a podcast and walk into a graduate level seminar on the

00:04:50.580 liver. But if you take a step back and think about it, we kind of need to, right? It is arguably one

00:04:55.380 of the most important organs in the body. It is certainly an organ as we discuss for which we have

00:05:00.900 no extracorporeal support. Meaning if your kidneys fail, God forbid, that's very bad, but at least you

00:05:06.640 have the option of dialysis. If your lungs fail, again, not a good thing, but at least you have a

00:05:11.540 ventilator. Even if your heart temporarily fails, we have ways to support that outside the body.

00:05:17.180 And yet remarkably, we don't have this for the liver. If a person goes into liver failure,

00:05:24.100 their only solution is a liver transplant. And what that speaks to obviously is the diversity

00:05:30.440 and complexity of function in this organ. So the role that it plays, and we really talked about

00:05:36.080 it in three categories, metabolism, protein synthesis, and detoxification. There simply is

00:05:41.420 no parallel for those things. Now we of course then talked about the role of alcohol. Everybody's

00:05:46.920 aware, of course, that alcohol is metabolized by the liver and therefore that excess alcohol is

00:05:53.320 toxic. But we talked a little bit about the how and the why, right? And that the metabolite of

00:05:57.720 ethanol known as acetyl aldehyde basically causes all of the downstream problems by overwhelming the

00:06:04.140 redox potential of cells in the liver. And that creates the attraction of free radicals and

00:06:09.760 inflammatory cells. We did a great job, I think, really just talking about dose makes the poison here.

00:06:15.560 So if a standard drink contains about 14 to 15 grams of ethanol, that will usually be found in

00:06:23.000 about 12 ounces of a regular beer. Interestingly, my favorite beer, which contains like 10% alcohol,

00:06:29.780 it would be, you'd get that 14 grams in far less. Five ounces of wine, one and a half ounces of liquor.

00:06:36.180 So if you're trying to think about how much ethanol you consume, you have to be mindful of the drink.

00:06:41.660 I noticed that when I'm pouring a glass of wine for myself or somebody else, it's never five ounces.

00:06:47.060 It's probably closer to eight. So I don't think it's intuitive for people to think about how many

00:06:52.140 grams of ethanol they're consuming. We didn't go much further into it here because we've done so

00:06:57.140 much other content, which we can link to in the show notes about the toxicity of ethanol based on

00:07:01.540 how many grams per day or grams per week you're consuming. Okay. Next major topic we got into

00:07:06.660 was that of what is called MAZL-D or metabolic dysfunction associated steatotic liver disease.

00:07:15.400 That's a mouthful. Why did we bring that up? Well, because you'll always hear me and for that matter,

00:07:20.780 many other people talking about NAFLD or non-alcoholic fatty liver disease. So this was an

00:07:27.080 education for me as well. And I think for the listener, which is we talk about NAFLD and that's been

00:07:32.980 something that's been talked about for the last 20 years, it's the fastest growing form of liver

00:07:37.460 disease in the developed world. And it's probably poised in its long-term sequelae to be the leading

00:07:43.740 indication for liver transplant within the next decade. But the reason that the liver societies and

00:07:50.600 the medical societies have taken on this name change is to basically be more encompassing.

00:07:57.000 So again, NAFLD has the intuitive point of saying, okay, it's a fatty liver disease that does not

00:08:04.180 result from the consumption of alcohol. Because of course, AFLD or alcoholic fatty liver disease

00:08:09.660 would be the sort of sister disease. But this idea of MAZLD or metabolic dysfunction associated

00:08:15.120 steatotic liver disease speaks to the complete overlap of insulin resistance, metabolic syndrome,

00:08:22.480 type 2 diabetes here. Now, to be clear, the overlap is so strong that I honestly think for those of you

00:08:30.040 as listeners, I don't know that it matters that much. According to Julia, 99.6% of people who meet

00:08:36.120 criteria for NAFLD will also have the diagnosis of MAZLD. So at that level, it's not really clear.

00:08:43.280 The diagnosis is based on metabolic dysfunction. So that's really the key thing when it comes to MAZLD

00:08:49.660 is you also have to have insulin resistance, but it does not require fibrosis. It requires also that

00:08:55.000 at least 5% of the hepatocytes, so hepatocytes are the liver cells, it's the functional unit of the

00:09:00.640 liver, they have to contain fat. One of the things that we talked about that I used to know, and this

00:09:06.060 is a great example of doing this podcast, is like there were things I once knew and then I kind of

00:09:10.040 forgot. And this was one of them, was about the difference between kids and adults and the different

00:09:14.740 pattern of fibrosis that they have. So in kids, it's more circulated around the portal vein.

00:09:22.540 The portal vein, again, this is maybe a little more in the weeds than people want, but for me,

00:09:26.220 it was very interesting. The portal vein is the vein that brings the majority of the nutrients

00:09:32.440 to the liver. So the portal vein is formed by the confluence of two enormous veins in the abdomen,

00:09:39.560 the superior mesenteric vein, and the splenic vein. And so they merge together and run into the liver,

00:09:46.960 and that's carrying just tons of nutrients into the liver. And in that sense, the liver has two

00:09:53.160 blood flows that are coming into it, one through the portal vein and one through the hepatic artery.

00:09:58.500 So what's the implication of this? Well, the anatomy of it notwithstanding, what's the implication

00:10:02.480 is what do you see from a diagnosis perspective? And in kids, you're going to see an earlier increase

00:10:11.040 in ALT, AST, and GGT. Now, again, you'll often hear these things referred to as liver function

00:10:19.080 tests. We talk about how we accept that as terminology, but the reality of it is they really

00:10:23.940 tell us nothing about liver function. They are enzymes that are associated with liver or hepatocyte

00:10:30.540 health. And when those enzymes go up, we generally understand that some sort of injury has taken

00:10:36.000 place. We'll talk about that more in a moment. In adults, the fibrosis and steatosis tends to occur

00:10:42.740 closer to the central vein. And as a result of that, you see a delay in the enzyme elevation.

00:10:50.280 So what does that mean clinically? It means that if you're an adult and you're developing steatosis

00:10:54.780 and fibrosis, it could actually be taking place for quite a while before you see it. And that's

00:11:01.660 why another huge takeaway, which I'll get to in more detail in a moment, is that this reliance

00:11:07.220 on elevations of the transaminases, which are the technical names for ALT and AST, and using that as

00:11:14.440 your threshold for concern might be waiting a little bit too long. Okay. So now if you look at the

00:11:21.900 top three causes of liver injury in the form of steatosis and fibrosis, you have Masaldi number

00:11:28.920 one, followed by alcoholic liver disease, again, something we should never forget. And then finally,

00:11:35.500 infections of which hepatitis is the most common. And real quick on that, Peter, just so people

00:11:41.980 understand is we had an older episode with Chris Sonnende on organ transplantation. And back in that

00:11:48.480 episode, you all talked about the liver, but the fact that Masaldi is now number one is something

00:11:54.460 that wasn't even close to true 20, 30, 40 years ago, correct? Yes. In fact, I even write about this

00:12:01.200 a little bit and outlive that I recount a story when I got either a medical student or an intern

00:12:07.160 more than 20 years ago, operating on a patient. And one of the jobs, I think it was when I was an intern,

00:12:13.980 because one of the jobs of the intern is to pre-op the patient. Pre-op the patient means get them

00:12:17.960 ready for surgery. And among those things is understanding how much alcohol they consume.

00:12:22.760 Because when a patient is undergoing major abdominal surgery, as was this patient for the

00:12:26.820 resection of a colon cancer, alcohol withdrawal, it's a very serious medical complication. So

00:12:32.140 patients who are drinking three or four drinks a day when they're in the hospital will either need

00:12:37.480 to have a continuous infusion of ethanol, or they'll have to have more benzodiazepines to cope with

00:12:42.540 the withdrawal, which can actually be fatal. So point of it is, you better understand how much alcohol

00:12:47.440 your patient drinks. And I'm talking to this guy the night before surgery, and he's telling me he

00:12:52.240 doesn't drink anything. Okay, great. Whatever. I ask you in a de-arming way. It's not like,

00:12:56.160 these are questions that people typically answer without reservation. We get into the operating room

00:13:00.620 to do surgery on this guy, and his liver looks like it's a piece of fat. And at the time, I think

00:13:07.460 everybody just assumed, A, I was a moron for not finding this out ahead of time. And B, once they 0.97

00:13:13.280 realized, yes, I did in fact ask that he was lying. And in fact, what I now realize, because we never

00:13:18.600 really gave it another thought, I wish I could tell you like this led to some lifetime journey

00:13:22.900 of mine to understand it. It was just, all right, let's get his colon out and make sure his cancer's

00:13:27.040 gone. But I now look back and realize this guy clearly had what we would have at the time called

00:13:31.440 NAFLD. So that's a long-winded way of saying you're absolutely right. 20 to 25 years ago, this was

00:13:37.080 really not something that was recognized, although it was probably far more prevalent than we believed.

00:13:42.980 But I would say that by, I would say 2010 to 2012, most people felt like this is an epidemic,

00:13:50.060 and this is going to be an enormous burden on the healthcare system as far as liver transplantation.

00:13:55.460 Again, getting back to the point at the outset, which is that extracorporeal support of a dysfunctional

00:14:01.640 liver is not possible. So we should spend just a second talking about hep B and hep C.

00:14:06.520 Obviously, people have heard of those things. For hep B, we do have a vaccine today. For hep C,

00:14:12.120 we do not. Conversely, for hep C, we have a treatment, whereas for hep B, we do not.

00:14:17.820 So the net-net is if you're someone who's coming of age today, you're a teenager today,

00:14:23.080 you're probably going to have a hep B vaccination, which is going to protect you from that. And should

00:14:28.680 you contract hep C, you're going to have a treatment. However, there are many people for whom

00:14:34.500 hep B was acquired before a vaccination was prevalent. And why do we care about this? Well,

00:14:39.300 we care about it for two reasons primarily. The first is the risk of liver failure and all of the

00:14:45.920 things we talk about through this pathway of steatosis, fibrosis, and ultimately what is called

00:14:50.860 cirrhosis, the irreversible fibrotic change of the liver. But the other thing we have to talk about

00:14:56.080 here is hepatocellular carcinoma, which is a deadly type of cancer if not caught very, very early. And

00:15:03.240 so the cancer risk here is a greater issue from the infectious side. So you always want to be

00:15:09.720 screening patients for hep C and hep B regardless of the workup. So in other words, when we're working

00:15:15.760 patients up for usually the first thing we're seeing is this elevation in transaminases, we're

00:15:21.720 also including a hep C and a hep B workup. The other thing to keep in mind here is that

00:15:27.460 Masal-D and alcoholic liver disease are also increasing the risk of hepatocellular carcinoma.

00:15:33.660 So it's not just hep B and hep C. And as a general rule, again, this was something I learned in the

00:15:39.260 podcast, either I'd forgotten it or never knew it, that as the scarring and fibrosis of any of these

00:15:45.840 diseases, Masal-D, alcoholic liver disease, hep C, hep B, as the degree of scarring and fibrosis,

00:15:52.000 increases, so too does the risk of cancer. And by the way, I misspoke there a little bit.

00:15:57.060 For hep B, that risk is regardless of disease progression. So let me just restate that. So

00:16:02.540 hep B, you're going to see about a 3% to 5% per year cancer risk, regardless of where you are in

00:16:08.640 the disease. So fortunately, again, we have a vaccine to reduce your risk of that. But for the others,

00:16:14.540 the risk of cancer goes up with the risk of disease. Okay. I think the last thing to talk about on this

00:16:20.640 topic is how do you make the diagnosis? Because the gold standard for this is to do a biopsy.

00:16:27.140 And it's not that a liver biopsy is as complicated as a cardiac biopsy or even a lung biopsy, but

00:16:32.460 that's not a procedure you would just go and do willy-nilly to stick a needle into the liver

00:16:36.400 with its risk of bleeding primarily or also infection. So really what we want to do is understand

00:16:40.840 how to make this diagnosis non-invasively. So look, again, nobody wants to do a liver biopsy.

00:16:46.680 So we're really talking about blood-based biomarkers and radiographic or imaging modalities.

00:16:52.980 Let's start with the blood-based biomarkers. If we're now going to look at blood-based biomarkers,

00:16:57.520 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

00:17:09.660 slash NAFLD with those biomarkers. Now, the reason that we see an elevation of these during

00:17:18.240 fat accumulation and or fibrosis in the liver is that these are enzymes made by the hepatocytes

00:17:24.160 that are released into plasma when the liver is stressed. So as you see more ALT and AST,

00:17:30.660 that indicates more stress. But it gets a little complicated because AST is also found in muscle.

00:17:36.100 And therefore, as you exercise, you will also see more AST increased into the plasma. And in fact,

00:17:43.900 that's one of the things we use to try to understand this. My AST is always higher than my ALT.

00:17:50.440 My ALT is typically in the mid to high 20s. And my AST is typically in the low to mid 30s. That is the

00:18:01.180 typical pattern for me and for many of our patients. And we know that that is a pattern that is pretty

00:18:08.260 typical of people who are doing quite a bit of exercise. The general rule of thumb is that you

00:18:15.360 would like to see an AST and ALT both below about 30 IU per liter. Again, I just told you that my AST

00:18:24.120 is typically a little bit above that. Normal results for me might be an ALT of 25 or 26 and an AST of

00:18:30.880 33 or 34. Am I concerned about that? No. I've obviously, being a curious person, done some more

00:18:37.800 imaging stuff to make sure there's nothing going on. But ultimately, you just have to handle each of

00:18:43.020 these situations kind of clinically. There are also pharmacologic things that will raise them. So

00:18:47.580 lipid lowering drugs are a very common offender and will raise AST and ALT. What is the threshold

00:18:54.440 at which you should be concerned? If you typically see somewhere between a one and a half and twofold

00:18:59.580 persistent increase, that would really justify investigation. Even if it's in response to a

00:19:05.420 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

00:19:19.920 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

00:20:16.340 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

00:20:51.700 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?

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00:28:01.060 Thank you.

00:28:02.060 Thank you.

00:28:03.060 Thank you.

The Peter Attia Drive - September 30, 2024

#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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