#162 - Sarah Hallberg, D.O., M.S.: Treating metabolic disease, & a personal journey through cancer

1. 0:00 – 0:10

   Intro

   1. PAPeter Attia0:00

      [upbeat music] Hey, everyone. Welcome to the Drive Podcast. I'm your host, Peter Attia. [upbeat music]

2. 0:10 – 13:30

   How Sarah discovered the profound impact of carbohydrate restriction for reversing obesity and type 2 diabetes

   1. PAPeter Attia0:10

      Hey, Sarah. Welcome to the show. I'm super excited to be speaking with you today. Um, this has the potential, of course, to be a 10-hour podcast, which it won't be, but I think that speaks to the, um, the depth of insight that you've got into so many topics that I actually wanna talk about. So, um, i-

   2. SHSarah Hallberg0:29

      Thank you.

   3. PAPeter Attia0:30

      [laughs] Yeah. In, in thi-

   4. SHSarah Hallberg0:30

      It's great to be here

   5. PAPeter Attia0:31

      ... well, in thinking long and hard about, um, how to sort of navigate all the threads I wanna pull on, I figured we would just start with the nerdiest of all topics, um, which is something that I know you're so passionate about, and yet, um, I don't think gets nearly enough attention. And that is basically the role of dietary intake of both carbohydrate and fats and the relationship that has on the distribution of fatty acids within the body. So let me just start by asking, like, why is that even of interest to you?

   6. SHSarah Hallberg1:08

      Well, I mean, it's significant interest because it really hits at one of the things people criticize a low-carb, high-fat diet about, is, "Oh my goodness, you know, you'll, uh, get more fat in your muscles, in your liver, and it's gonna lead to increased insulin resistance and thereby default going to lead to increased cardiovascular disease." And we know that, um, a therapeutic carbohydrate restricted diet, um, brings down so many, um, cardiovascular risk biomarkers that we're all used to hearing about. Okay, it decreases triglycerides, you know. Okay, it actually can reverse Type 2 diabetes, um, in most cases, and certainly significantly improve glycemic control, um, in all. Um, but fatty acids, that's not something that's talked about all that often. And what is talked about all that often is this idea of you are what you eat, right? We hear that still every day. "Remember, you are what you eat." And this example of what happens when you consume saturated fat in the matrix of a diet that includes carbohydrate restriction is so against that long, worn out idea of you are what you eat. And so fatty acids play a critical role, study after study will show us, in cardiovascular risk, um, and in future diabetes risk as well. But again, it's, it's not discussed because fatty acids are confusing. Let's face it, okay? And most people would rather just fall back on this idea, you are what you eat, which just really flies counter to what the evidence in the peer-reviewed published literature says.

   7. PAPeter Attia3:16

      So maybe taking even a greater step back from that, uh, Sarah, what is it, um, that attracted you personally as a physician towards the management of Type 2 diabetes? Because, uh, I mean, that's how you and I got to know each other, was through a company that you- you're a big part of, uh, called Virta Health, which I'm sure at some point today we will talk about. Um, but what attracted you to this patient population, and how is it that you stumbled upon the idea that there was, uh, perhaps another way to treat patients with Type 2 diabetes that was not kind of the standard treatment, which was chasing glycemic control with insulin or insulin-increasing, uh, drugs?

   8. SHSarah Hallberg4:06

      Well, I tell you, it's by accident. Um, if you had told me 20 years ago that I'd be playing this role in the healthcare system, um, I probably wouldn't have believed you. Um, so it goes back again to the fact that for a very long time... I mean, I've been in the world of obesity care for well over 25 years now, and just the first half of that was telling people that the way to fix everything was to eat a low-calorie, low-fat diet. Um, you know, I grew up as a product of the '80s, like so many people, where that was, you know, that was the dogma. There was no other way. And of course, entering into college and, um, grad school, where I, um, got both my bachelor's and master's in exercise physiology, I mean, that's what we were taught. Moving on to med school, you know, reaffirmed once again. So when I went into practice as a primary care physician, um, I'm board certified in internal medicine, um, it was more the same. But again, it was so frustrating to me, you know, all along the way really to be continually giving this advice and then have people show up being worse, you know? I'm not making them healthier. I'm making them... or I'm watching them become more unhealthy, and that was depressing, and it was really quickly became just to the point where it was like I, I, I can't continue on with primary care for the rest of my life because I felt like a legal drug dealer. I got really lucky here, okay? Um, I, I like to say a lot of my pivots are pivoted on anger, right? Pivots in my career, and I was really angry at what was happening on the primary care level. Um, and as luck would hapit- have it, um, at Indiana University Health, they knew about my background, knew about my past work in obesity care and asked me to start a program, uh, obesity program, and I jumped at the opportunity And I was lucky to be able to take some time off over the next year, spend time figuring out what, what was this gonna look like, you know? How were we gonna tackle the untack- tacklable, if you will, problem, you know, that is obesity. And I started sticking my nose in the literature, which is something that every physician wants to do, but not every physician is afforded the time. Let's face it, you know, we are just boom, boom, boom, see patients. There's th- just such a busy lifestyle in everything right now. But I was given a chance to step back some, so I had time to prepare for this. And in that, I discovered carbohydrate restriction as a means to weight loss initially. Um, listened to some lectures by Dr. Steve Phinney and Jeff Volek, um, and I was like, "Whoa, that makes total physiologic sense." And so boy did I dig deeper into this. I read everything I could get my hands on and really came to the conclusion, which required a lot of, you know, cognitive dissidence overcoming, that what I had been saying, you know, for well over a decade to so many people was really not founded on good science, and that the field of carbohydrate restriction, while still relatively in its infancy at the time, showed much more promise. And so we opened the clinic as a carbohydrate restricted clinic, but the fact of the matter is, although people were losing weight, what we were so- seeing that was so much more meaningful was that people's diabetes was, like, going away. They were having normal blood sugar. We were pulling them off of insulin at rates that I could never have believed had I not been the physician who was taking care of these patients. I mean, it was astronomical.

   9. PAPeter Attia8:22

      Now, Sarah, just a couple questions.

   10. SHSarah Hallberg8:24

       Hundreds of units of insulin.

   11. PAPeter Attia8:25

       Uh, d- sorry

   12. SHSarah Hallberg8:25

       Yeah

   13. PAPeter Attia8:25

       ... just to, just to interject, um, w- did you... First of all, there's two questions I guess I want to ask you. One, were these patients primarily patients with type 2 diabetes, or was it primarily obesity, of which a subset had diabetes? And secondly, how much resistance did you have in your own institution when you showed up and said, "Hey, I know you guys brought me in to do this thing. I'm gonna do it, but oh, by the way, my secret sauce is gonna be this," at the time, very unconventional approach?

   14. SHSarah Hallberg8:52

       Great question. So as you probably can imagine, when, uh, patients come into an obesity clinic, um, most all of them, if not all of them, have some form of metabolic disease, um, you know, the m- the biggest being type 2 diabetes. So we were seeing type 2 diabetes all of the time, consistently, daily. And you're right, I had to take precautions because, again, this was 10 years ago, and not as much about carbohydrate restriction was known at that time, certainly among general practicing physicians in any discipline really. And so I knew that I had to head off the potential resistance that was gonna come. There was just no question of it. So I actually went about and spent an entire summer meeting with all the departments in, um, our local med center and giving them a 15-minute slide presentation of when your patient comes back, says that Dr. Hallberg told them to eat a lot of fat and not a lot of carbohydrates, that I wasn't crazy, that this was actually based on evidence, and here it was. And you know, Peter, you'd be surprised. I, I didn't get any pushback. I actually pushed it even to the next level. I was part at that time of the Ambulatory Quality Committee at our institution, and I actually brought up a, uh, amendment that all patients with metabolic disease should at least be provided the option of trying this if they wanted, and it passed unanimously. I mean, people got it. Once they had time to pause, take a look at the physiology behind this, and realize, "Okay, yeah, that makes a lot of sense." So it changed my life, right? And again, I, I like to always say my career is built of inflection points of anger, and as we were seeing these huge changes of diabetes and patients just resolving their diabetes, I became really angry 'cause I was like, "Where is this? Where is this in the guidelines? How come I've never heard of this before?" I mean, this is, you know... I, I mean, I hate to be, like, overdramatic, but it truly is quite miraculous. For a disease that everyone thought was chronic and progressive, to see people recover from it, um, is quite astounding. And so I decided that I needed to get into research. So actually to start off with, I called Purdue University's nutrition pro- program and asked one of the researchers there if they wanted to help me on just an early unfunded pilot study to prove my point, looking at metabolic improvements and looking at financial improvements too because obviously if people weren't taking all this medicine, they weren't costing themselves and of course the healthcare system as a whole as much money. And so I talked about that study, presented it at the National Lipid Association quite a long time ago, talked about it actually in my TED Talk, um, and then was speaking at the Obesity Medicine Association quite a long time ago and actually met Dr. Steve Phinney, um, and that really changed the course of my life as well.

   15. PAPeter Attia12:26

       So all this time you're sort of putting into practice what Steve and Jeff had been writing about for a long time. And, and obviously, uh, Steve is someone I've been, you know, dying to have on the podcast, and we were actually supposed to do it at, uh, at one point in time, and then scheduling got in the way. Um, but, um, I didn't realize that you had already sort of gone down this path and yet hadn't actually met him, because I took the opposite approach, which was when I started kind of implementing some of these treatments, you know, I'm just a bull in a China shop. I just reached out to Steve right away. Um, I, I might have been one of the first people to get a copy of the, uh, the book that he and Jeff wrote in 2011. I think I got a preprint of that book, which I still have, by the way.

   16. SHSarah Hallberg13:10

       The Art and Science?

   17. PAPeter Attia13:10

       The Art and Science book, which I have.

   18. SHSarah Hallberg13:12

       Mm-hmm.

   19. PAPeter Attia13:12

       It might have more highlights and Post-its in it than any book I own. Uh, because I think, like you, I was kind of going through the, "This can't be. Something... There's something that's not... Um, there's something so counterintuitive to this that I, I, I need to read this over and over and over again to

3. 13:30 – 27:45

   Prediabetes and metabolic syndrome: prevalence, early signs, and the importance of treating early

   1. PAPeter Attia13:30

      make sure I get it." Um, so it's funny that, that that's the case. Now tell me, where did... You know, were you at this time going to ADA meetings, the American Diabetes Association meetings? And, and, and when you would discuss what you were seeing in your practice with your peers, who were also on the front lines taking a more traditional approach, uh, how was your experience being... Uh, how, how was that met?

   2. SHSarah Hallberg13:56

      Well, it's interesting. If someone... If I was speaking with someone who took care of obesity patients for obesity, they were totally, "I get it. You know? Uh, y- I'm doing the same thing to some varying degree." But when you moved out of that space to other subspecialists, um, the first thing was, "Oh, yeah, their diabetes will go away, but you're gonna kill them with heart disease," right? Or, "Oh, you know, we all know it works." I'll never forget one of the leaders in the endocrine movement said, "Look, we all know it works. This is not a secret, but nobody can stay with it." And I was like, "I... You know, I don't know. Here in my practice, I have thousands of patients that would beg to differ with that." Um, and so, you know, those are the feedback that I got. And so one of the things was I knew that there had to be even more research done. I mean, you know, we had wonderful pioneers in, you know, Steve and Jeff and, um, s- Eric, um, from Duke, Westman. Um, but we needed even more. They needed to be larger trials. They needed to really specifically focus on patients with type 2 diabetes, 'cause I was convinced almost from the get-go that that is the target population here, because that's where we see the biggest improvements. And so this ch- chance meeting, um, with Steve at a Obesity Medicine Association conference led to a dinner and led to funding of the large clinical trial that we're actually wrapping up in the next couple of months. Right now, we're at the tail end of our five-year data collection of the longest and largest trial, um, looking at, um, nutritional ketosis as a means of reversing type 2 diabetes and prediabetes, which I'll just kind of stick in really quick here. Um, today actually happens to be the day that the prediabetes paper was published. So I'm really proud to say this is the eighth paper already that's come out of this large trial, started by a chance encounter, um, at a conference. And, um, the... We haven't published the prediabetes results until today. So this was a, um, a paper that looks at the first two years of prediabetes, um, utilizing a remote continuous support to help patients adhere to a diet aimed at nutritional ketosis.

   3. PAPeter Attia16:41

      And Sarah, these are, the- these are patients defined as prediabetic by hemoglobin A1C?

   4. SHSarah Hallberg16:48

      Correct.

   5. PAPeter Attia16:49

      And that's, um-

   6. SHSarah Hallberg16:50

      Correct

   7. PAPeter Attia16:50

      ... in the... That's being defined as 5.7 to 6.4? Is that the range?

   8. SHSarah Hallberg16:56

      That's correct.

   9. PAPeter Attia16:57

      Okay.

   10. SHSarah Hallberg16:57

       Yes.

   11. PAPeter Attia16:58

       Tell people what that means. Um, I think most people are aware of what a hemoglobin A- A1C is, but, um, what does that translate to in an average glucose approximately?

   12. SHSarah Hallberg17:07

       Yeah, so we really start to get... For example, fasting, that's the one most people are familiar with. And once you get a fasting glucose over 110, you know, that's the worrisome prediabetes range. And I, I do have to say here, though, that doesn't mean normal glucoses are okay for everyone. And I think you've had, you know, many people on here talking about the perils of insulin resistance and how it starts to cause significant problems in people who still have normal blood sugars, and I just think that's such an important point and, and can't be overstated again. But in this study, we're looking at people who had insulin resistance long enough that their pancreas and the beta cells could not keep up with the insulin that was needed to keep blood sugar normal, and their blood sugar started to rise, not yet to the level where a diagnosis of type 2 diabetes could be made, but once again, where we see the impact of insulin resistance affecting the body's ability to keep blood sugar normal due to pancreas being overworked, um, for far too long.

   13. PAPeter Attia18:29

       And, and if we believe that- I mean, I don't know what the latest numbers are, but I'm guessing it's still about 10% of the US population has type 2 diabetes. Is that approximately correct, or is it... Are we more than 10% now?

   14. SHSarah Hallberg18:42

       Approximately, with also the caveat of much more concerning levels in different minority populations, which of course, um, hopefully we'll get a chance to talk about later, is just a huge goal with improving health equity in this country.

   15. PAPeter Attia19:01

       So if it's 10% in all comers, do you have a sense of what it is in Hispanic and African American populations?

   16. SHSarah Hallberg19:07

       Yeah, it gets even higher. It's well into the teens in those, and Pacific Islanders as well. So these are populations that, you know, we need to be paying attention, of course, to everyone who has type 2 diabetes, but we also need to be paying attention to who's at greater risk.

   17. PAPeter Attia19:24

       So what percentage of the population do we believe is in the predi- formally in the prediabetic camp? Which again, I think what you said a moment ago is very important for people to understand. If we go back to the podcast with Gerry Shulman, um, which is one of my favorite discussions ever on the topic of insulin resistance, I mean, Gerry really laid out elegantly, um, the long time course of this disease. And even, you know, even if you have normal fasting glucose and fasting insulin, but that early sign of elevated postprandial insulin is really that early sign of insulin resistance that will then lead to postprandial glucose elevations, and even that can still exist in the presence of normal fasting glucose. So to your point, by the time someone registers as a prediabetic, quote-unquote, I mean, this has been a process that's been going on for five to 10 years, what s- what, what is the... What, what is our belief about how many or what percentage of Americans, just to make it, you know, American-centric for a moment, what percentage of Americans are in that bucket?

   18. SHSarah Hallberg20:31

       Well, I tell you, you know, studies, recent studies all show us that over 50% of Americans, adult Americans, have diabetes or prediabetes. And a study released a couple of years ago, and I mean, this, this should shock everyone to its core, based on NHANES data, that 88% of Americans are not in optimal metabolic health. I mean, let me say that again. 88% of adult Americans are not in optimal metabolic health, and that is by looking at NHANES data and taking a look at the criteria for metabolic syndrome. And so, you know, the 12% are those who didn't meet any of the criteria for metabolic syndrome.

   19. PAPeter Attia21:19

       Okay.

   20. SHSarah Hallberg21:20

       I mean, that's frightening.

   21. PAPeter Attia21:21

       Yeah, so I was gonna, I was gonna ask you an- if that's exactly what it meant. So just let's state for the, for the listener what metabolic syndrome is. We've certainly discussed it on this podcast, but it would be great to remind people what are those 12% doing? They have none of the following five, right? They have normal blood pressure. No, they do not have elevated blood pressure. And again, um-

   22. SHSarah Hallberg21:42

       And they're not on medication

   23. PAPeter Attia21:43

       ... and they're not taking medication to lower blood pressure. And normal is now being much more stringently defined, but I believe the latest CDC definition of normal is less than 130 over 80. Um, in our practice, we advocate less than 120 over 80. They have normal fasting glucose, and that's defined as less than 100. Um, they have normal triglycerides, which are being defined as less than 150. We argue in our practice that's very high, and anything over 100 is elevated.

   24. SHSarah Hallberg22:16

       Totally agree.

   25. PAPeter Attia22:16

       They have normal HDL cholesterol, which for men is defined as greater than 40 milligrams per deciliter, for women greater than 50 milligrams per deciliter. And they do not have truncal obesity, and I forget, I think for men, that's defined as 40 inches of waist circumference, in women 36. I don't know if that's, uh, if that's still the latest.

   26. SHSarah Hallberg22:38

       Well, yeah, and I will also point out one really important thing here when it comes to waist circumference, too, um, and the definition of metabolic syndrome, and it little bit goes back to what I was saying before about the consideration of minorities and different ethnic populations, which is we have to take the, um, uh, that into account even when we're defining metabolic syndrome. Because for Southeast Asians, they are defined as having metabolic syndrome at a much lower waist circumference. And for African Americans, we need to really consider as well because they tend, even in the face of having, um, insulin resistance, they tend to have normal triglycerides and HDL. And so again, you know, we can't be treating everybody the same, but we often do.

   27. PAPeter Attia23:41

       Yeah, I'm glad you pointed that out. I, I, I still remember, it's, it was about 10 years ago when I learned that lesson, which was, you know, taking care of an African American patient who had about the most uncontrolled diabetes I'd ever seen. You know, hemoglobin A1c of 14%. This is a person who's basically gonna have their limbs amputated in the next hour. Triglycerides of 89, just-

   28. SHSarah Hallberg24:06

       Oh, yeah

   29. PAPeter Attia24:06

       ... yeah, just totally normal. You look at their lipid panel, you wouldn't think anything is wrong.

   30. SHSarah Hallberg24:12

       Right. And so th- that's the thing, is they can get missed.
4. 27:45 – 33:45

   Overview of fatty acids, how they are metabolized, and understanding what you see in a standard blood panel

   1. SHSarah Hallberg27:45

      really explore.

   2. PAPeter Attia27:46

      Yeah, indeed. So with that background, let's kind of dive into some of this nerdy, nerdy fatty acid stuff. And, and I gotta tell you, I find this stuff really interesting in part because I think it's complicated enough to make sense of just the eating side of this stuff. In other words, um, you know, just for the listener, you know, I think people that have listened to this podcast, we've done a number of shows that have dealt with fatty acids. People probably understand that there are saturated fats, monounsaturated fats, and polyunsaturated fats. Um, the saturated fats have no double bonds, so that means every carbon is fully saturated with hydrogen. The monounsaturates have one and only one unsaturation, um, so one double bond. And then the polys have at least two of these double bonds. But it's the manner in which these things can be made from each other that becomes quite interesting, isn't it? It's really the way that you can ingest one form, and it can be turned into another. So I'm wondering if the easiest place to begin this discussion is to introduce what the fate of a very common fat in our body is, um, which is the C16 saturated fat. So can you talk a little bit about how abundant that is, um, and what our body's options are for it? What it's called. Let's start with the nomenclature. What is, what is C- what does pure C16 look like?

   3. SHSarah Hallberg29:26

      That's palmitol- palmitoleic acid. Um, and, um, so it's really interesting what happens. And do you mind if I jump on and share screen here-

   4. PAPeter Attia29:37

      Yes, please

   5. SHSarah Hallberg29:37

      ... so we can talk a little bit more about it?

   6. PAPeter Attia29:38

      Yeah, that would make it easier for everybody, I'm sure.

   7. SHSarah Hallberg29:42

      I wanna start by talking about, um, saturated fatty acids in general, okay? And what we know is that going back here to the basics and looking at the liver, when we have incorporation of saturated fatty acids into our triglycerides, okay, that is correlated with insulin resistance and adiposity, okay? Likely reflecting accelerated hepatic de novo lipogenesis, okay? Or also it can be what is actually returned to the liver, so really two. Um, we certainly know that hepatic de novo lipogenesis is a, a big part of the problem, um, when it comes to elevated triglycerides, but we can also make these with some, uh, what is delivered exactly back to the liver. And so when we see saturated fatty acids, okay, as a makeup of triglycerides or maybe even the phospholipids there, um, we say, "Oh my goodness, that's a marker of increased saturated fatty acid consumption," right? These people are eating a high saturated fat diet. And that seems to make sense, and this is the problem with a lot of things in science in general, um, but, and nutrition science is no different, is that just because it seems to make sense doesn't mean it's the way things actually work, okay?

   8. PAPeter Attia31:17

      Sarah, can I-

   9. SHSarah Hallberg31:18

      And so-

   10. PAPeter Attia31:18

       Can I explain a technical point on this slide that you and I will take for granted-

   11. SHSarah Hallberg31:22

       Sure

   12. PAPeter Attia31:22

       ... but I want to make sure that a listener understands?

   13. SHSarah Hallberg31:24

       Absolutely. Please do.

   14. PAPeter Attia31:26

       So when, when a patient goes and gets their blood drawn, let's just say they get a standard lipid panel. It will spit out the following values. Total cholesterol equals 200 milligrams per deciliter. LDL cholesterol equals, you know, 140 milligrams per deciliter. Triglycerides equal 150 milligrams per deciliter. HDL cholesterol is 35 milligrams per deciliter. And VLDL cholesterol, if I remember the numbers I just spit out, would be 25 milligrams per deciliter. In other words, the VLDL cholesterol, HDL cholesterol, and LDL cholesterol sum to the total, and then the triglycerides are independent. What I want to make sure people understand is those are all found within the lipoproteins. So VLDL cholesterol is the amount of cholesterol ester contained within the very low density lipoprotein. LDL cholesterol is the total content of cholesterol ester found within the low density lipoprotein, et cetera, for the HDL. Here's the part that's really interesting. We always check these things fasting because we-- when it comes to measuring a triglyceride, we want to eliminate what's in the chylomicron. We want to eliminate the immediately absorbed triglyceride from the gut. And by doing that, we basically capture what you have on this photo. When we measure a triglyceride, for all intents and purposes, we are basically measuring the 90% of triglycerides that are captured within the VLDL. So, um, let me restate that 'cause that was a bit rambling. When you go to the doctor and get your blood tested and it says your triglycerides are 150 milligrams per deciliter, that's basically saying, look, 90% of that 150 milligrams per deciliter is within your VLDL cholesterol. I-- There's some of that is in intermediate density lipoprotein, but that's virtually non-existent. There's a trace of that in the LDL cholesterol and even a smaller trace, uh, in the HDL. Um, but it's-- the lion's share is in the VLDL cholesterol. And as you're going to explain to us, this process of de novo lipogenesis, the conduit from fat being made in the liver and exported, that conduit is the VLDL particle. That's,

5. 33:45 – 47:50

   The relationship between diet composition and metabolic markers

   1. PAPeter Attia33:45

      that's going to become very important in this discussion.

   2. SHSarah Hallberg33:47

      Absolutely. Absolutely. Um, yeah, and that's really important. Thank you for the, the precursor explanation 'cause it is real-- this is technical stuff, and that is really important, um, for people to understand. And so, you know, then the next question really becomes, okay, so if we have a high saturated fatty acid content within the VLDL, okay, um, again, it's being in the triglycerides, the phospho, uh, lipid membrane, um, we c- wherever we find it. Where did the saturated fatty acids come from? Um, is it directly from consumption? And I just want to first point out before we get into maybe more of the technical stuff some of the clinical trials that can help us understand this a little bit better. And so this is one of my favorites, um, by Dr. Brittany Volk, um, that was published a while ago, and it's really great because this was a feeding study. So, you know, they kept track of what the patients were eating. It wasn't a free-for-all. Are they eating what they're-- we're telling them to eat or not? They provided all of their food. And this was patients with metabolic syndrome. They went through six feeding phases. And so they did a run-in with a very low carbohydrate diet for everyone, less than 50 grams of carbohydrates a day. And every three weeks, they increased the carbohydrates in the diet all the way up to, uh, 346 grams, which was C6 feeding phase. And the other thing to note here is the saturated fat content. So when we were at the low carbohydrate end here in C1, they were consuming 84 grams of saturated fatty acids a day. Okay? So that blows away any, um, guideline on saturated fat, I mean, so far above what anyone would consider, um, a g- at goal. And then we get down to the C6, and we're much less, 32 grams. Um, again, uh, what happens to the fatty acids as people are run through these six phases?

   3. PAPeter Attia36:16

      And, and Sarah, just to be clear, this is basically an isocaloric feeding study, which means as you're ratcheting up the content of carbohydrate, you're commensurately reducing at a caloric level the amount of saturated fat, right? I believe this study did not change the number of calories they were consuming. Or did it?

   4. SHSarah Hallberg36:39

      Correct.

   5. PAPeter Attia36:40

      Okay.

   6. SHSarah Hallberg36:40

      They did not. Okay? And so what happened, um, to the, um, saturated fatty acid levels in the blood, and for that matter, others, other fatty acid levels in the blood? So what happened over these six phases? Okay. So here we have saturated fatty acid levels marked. Okay, so here's the baseline at that run-in. Okay. And we see when we have the very high saturated fat level, very low carbohydrate. Okay. Here we go. And what's really interesting is what happens as we march along here down to C6. And if you remember, this is much lower saturated fatty acid content of the diet. Okay. Um, much higher carbohydrate intake. What we see is that it's actually the saturated fatty acid content is actually higher with the lower saturated fat intake. And, and we're going to come back and talk to, about the science behind that. But I think it's really important for people to see this clinically, and then maybe when we get into a little bit more of the nitty gritty, um, it can make more sense. Okay.

   7. PAPeter Attia37:59

      I mean, it's, it's actually statistically insignificant in terms of-

   8. SHSarah Hallberg38:03

      Correct

   9. PAPeter Attia38:04

      ... C16, right? Which is the dominant saturated fatty acid. So, so palmitic acid, it trended towards an increase as saturated fat, dietary saturated fat went down, um, and sat- and c- carbohydrate went up, but it didn't reach significance. And, um, w- the only one that actually did significantly increase was C14, right?

   10. SHSarah Hallberg38:30

       Yeah. Actually, um, C16, one as well, and that one is we're going to spend-

   11. PAPeter Attia38:36

       Oh, oh, yes

   12. SHSarah Hallberg38:36

       ... hopefully a little bit of time on.

   13. PAPeter Attia38:37

       But, but, but, but yeah, yeah, yeah.

   14. SHSarah Hallberg38:38

       Okay.

   15. PAPeter Attia38:38

       No, but as a saturated fat, it was really just-

   16. SHSarah Hallberg38:41

       Oh, as a saturated fat.

   17. PAPeter Attia38:42

       Yeah, yeah.

   18. SHSarah Hallberg38:42

       Yes.

   19. PAPeter Attia38:42

       Yeah. So...

   20. SHSarah Hallberg38:44

       But the point of this is we didn't have these really high levels of serum saturated fatty acids when we were consuming, when these participants were consuming this-

   21. PAPeter Attia38:57

       Right

   22. SHSarah Hallberg38:57

       ... very high saturated fat diet.

   23. PAPeter Attia39:01

       Yeah.

   24. SHSarah Hallberg39:01

       I mean, essentially, and this is important, it stays the same.

   25. PAPeter Attia39:04

       Yeah.

   26. SHSarah Hallberg39:05

       If anything, there's a trend, okay, to higher serum saturated fat in the low fat arm. Okay. But certainly we do not see a rise in the high intake of saturated fat. That's super important. And again, it goes against what I was saying earlier on, you know, you are what you eat. Well, okay, if that's true, then when I consume a very high level of saturated fatty acids, why am I not seeing that again in the blood, in the serum? Why are we not seeing that?

   27. PAPeter Attia39:47

       And, and what's nice in this study is you've exhaustively looked at where the fatty acids are. So obviously the most efficient place we store fatty acids is in the triglyceride. Um, but you also store it within the cholesterol ester, and it's obs- obviously in the phospholipid as well. But regardless of where you look, you see no association between dietary saturated fat and fatty acid composition with respect to saturated fat.

   28. SHSarah Hallberg40:20

       That's right. That's right. And I want to really quick draw attention here to one more that we are going to be talking more about, and that's 16, one, that's palmitoleic acid. And we're going to talk more about why that's important. But as we can see here, when we follow that across, it significantly rises when we have less saturated fat and more carbohydrates. And you can see that is statistically significantly different in every place that we're looking. Okay. So moving on. When we take here a low saturated fat diet, low fat, low saturated fat diet, and we compare it to a low carbohydrate, high saturated fat diet over 12 weeks. This is from Jeff Volek's group from 2008. And what I like here is you can see very readily with these pie, uh, charts exactly what the content of the two diets were. So again, we really have it flipped, you know, high carbohydrate, low carbohydrate, low fat here on the left to a very high intake of fat on the right. And again, below it, the two different levels of saturated fat that we're comparing, 12 grams to three times as high in the low carb diet at 36. So then what happens again to the-

   29. PAPeter Attia41:56

       Sarah, these are both, these are both really low calorie studies. Was this an ad lib feeding study, or were these deliberately calorie restricted? Uh, h- h- how, how was this study done?

   30. SHSarah Hallberg42:09

       Yeah, these were both... They wanted the calorie intake of the two studies to be the same. So as you can see, they were about 1,500 calories a piece.
6. 47:50 – 1:00:30

   Why palmitoleic acid is such an important biomarker

   1. PAPeter Attia47:50

      let's now ask the question, Sarah, what is it about palmitoleic acid that you think is such an important biomarker? 'Cause we wouldn't be having this discussion if you didn't think we should be paying attention to this.

   2. SHSarah Hallberg48:06

      Yeah. I think it's a really important biomarker, and if, if you, if you would, um, allow me, let me point out one other thing here regarding the triglycerides because clearly the low carbohydrate arm decreased more in the triglycerides, okay? Um, the low fat arm decreased too, which may come as a surprise to your listeners because we do associate low fat with an increase in triglycerides. Um, but I do wanna remind everyone that this was a calorie restricted. That this was around 1,500 calories. So that drop in the low fat diet arm, although maybe not what we were expected, does make sense with the reduction in calories overall. Now let's go back and talk more about your question. Okay? I think palmitoleic acid, or again, that's that 16:1, um, is really not appreciated, um, as the health predictor that it really is. Okay? So let's go through... I'm gonna just jump ahead a little bit here. So palmitoleic, or w- we like to call it POA, is a product of something called stearoyl-CoA desaturase. Um, and stearoyl-CoA desaturase is going to, um, determine, um, what is going to happen with some of the fatty acids in our system, specifically what's gonna happen to POA. Now, what we know ahead is that stearoyl-CoA desaturase is actually an independent marker of triglyceridemia and abdominal adiposity. So in other words, an independent marker of all those things that go along with insulin resistance. All right? So if we have a high levels of stearoyl-CoA desaturase activity, you know, right there we gotta start thinking things may be concerning even if someone has a normal blood sugar, right? Because right now I think one of the important things based on our, the earlier part of our conversation where we say so many times these things are missed, you know, people can still have normal blood sugars, you know, it's gonna be really important, you know, number one, that we make everyone aware that a normal blood sugar doesn't mean that you are healthy, but number two, what are some easy ways and some easy markers maybe that we can check to know that we're headed for trouble even before we have blood sugar go up? Okay? So plasma, um, uh, triglycerides, and let's take a look at, um, again, POA in those plasma triglycerides in the way of looking at it in quartiles. Okay? So again, low versus high. And what we can see is the POA, all right, the byproduct, okay, of stearoyl-CoA desaturase is much higher the higher the triglycerides are. Okay? Very important. So if your triglycerides are really high, again, what's happening very likely is that your POA is elevated as well, okay, brought about by increased activity of stearoyl-CoA desaturase.

   3. PAPeter Attia51:52

      And this shouldn't be surprising, right? Because-

   4. SHSarah Hallberg51:55

      No

   5. PAPeter Attia51:55

      ... if you look at the very, you know, unfriendly diagrams of fatty acid metabolism, um, one of the first steps we see in the conversion of, or elongation of fatty acids is the conversion of C16:0 palmitic acid into C, uh, 16:1 palmitoleic acid N seven through an enzyme that has two names, I guess depending on the name of nomenclature, right? So delta nine desaturase desaturate the number nine carbon from the delta end, also known as stearoyl-CoA, uh, uh, saturase, uh, desaturase, which I think is the more popular name is, is SCD1, right?

   6. SHSarah Hallberg52:41

      Right.

   7. PAPeter Attia52:42

      And if you, and if you go down that pathway, what you're basically doing is bundling and packaging fat to leave the liver, right?

   8. SHSarah Hallberg52:51

      Yes. And, and, and here is one of the... That is an interesting point because the question is, if we're trying to change the serum saturated fats into something else, okay, I mean, the body is obviously doing that. One would have to wonder, is that a protection mechanism? Why do we wanna do that?

   9. PAPeter Attia53:16

      I, I, I... Yeah, I... To me that's a great question, Sarah. It seems counterintuitive if I'm going to be obvious because we would think that a saturated fat is much safer. It's inert. There's no chance a reactive oxygen species can be formed out of it. Uh, why is it our body, even if we wanted to export fat from the liver, which we could argue all the reasons that's not a great idea, why would we go to the trouble of this conversion?

   10. SHSarah Hallberg53:41

       All right. Well, let's go through it really quick and then get to answering that question 'cause I think it's really important and really sheds light on why we need to be paying more attention to the all important POA and, of course, the, um, precursors and, and, um, enzymes that, uh, act in its creation. So let's go through, if you will, this cartoon that I know looks really busy, um, initially. Um, but let me just kinda run through it starting here, um, in the intestine. And remember, you know, w- we'll start off by saying our focus in healthcare, um, and in nutrition recommendations for so long has been low fat, low fat, more carbohydrates, higher carbohydrates. Well, let's take a look in the intestine at those carbohydrates, changing the focus for a minute. So they come in rapidly absorbed carbohydrates or even our slowly absorbed carbohydrates, our starches. Okay? Um, and what happens when they come in, right? As glucose, um, that feeds in again through GLUT2 into the pancreas Pushing out more insulin. Insulin then feeds into the liver, and what we get here, okay, is going through it, a big, big part of this is SREBP-1, okay? And I don't know if we need to get that technical, but we'll lead here to that enzyme we were talking about, the SCD-1, um, uh, or stearoyl-CoA desaturase increasing. Okay? Very important. And it comes about through other means as well. Fructose coming in through GLUT5 or glucose coming directly into the liver through GLUT2. They're all feeding into this by slightly di- different mechanisms to increase this SCD-1. Now we're gonna look more at the process, um, in a different way. So we have increased hepatic, first of all, saturated fat. Okay? Here's our 16:0, the saturated fat. All right? C- uh, increased hepatic levels of this. What gets turned on, as from the past cartoon, we get that SCD-1 activity increasing. That leads to this increase in POA. All right? Coming down here, what's the end gain here? Increased VLDL. All right? Same thing over here, looking at it different. Um, we see again SCD-1, if it's blocked, we won't see that. All right? We'll see a decrease in VLDL, and this again has to do if this SCD enzyme is blocked, we're going to have an increase in the saturate, a decrease in our POA. Okay? But again, what we have when we're consuming the high carbohydrates, even if they're the, again, more refined carbohydrates or the less rapidly absorbed carbohydrates, this is the path that we wind up going on. 16:1 is, or 16:0, saturated fat is elevated, and it turns on this cascade leading to increase in VLDL. I'll pause there before we go on if you had any comments that you wanted to add here.

   11. PAPeter Attia57:45

       Yeah. Again, I think, uh, you know, for, for folks that are watching this, it's gonna make a bit more sense, and if you're not, I just wanna make sure we're, we're bringing you along for the ride. So, you know, in the liver, when you are taking C16 or C18, but let's just keep the discussion simple and start with a saturated C16, it's, it's, the first committed step is going through SCD-1 as an enzyme, and it adds that double bond. It makes a few more steps along the way, but ultimately it is increasing a process of lipogenesis. It is making more lipid. It is increasing the amount of lipid within the cholesterol ester and the triglyceride. It is being exported from the liver. So in response to your question, Sarah, is this protective, I guess the answer looks like the body is saying, "Well, gosh, I would rather get this fat out of the liver than keep it in the liver." And we know that it's not fully successful in doing that because of course, although it hasn't come up yet on this discussion, everything we've talked about today runs hand in hand with non-alcoholic fatty liver disease, which is truly an epidemic at the moment. Um, but I suspect that the body is still doing its best, even in the case of non-alcoholic fatty liver disease, to try to export this fat as much as possible. The triglyceride is a very efficient place to store it. Um, I've always believed obesity is a protective mechanism. I think that obesity is not the cause of metabolic illness, but the result of it, um, which is not to say that the inflammatory environment that comes with it doesn't pour more gasoline on that fire. But I... You know, it is my belief, um, that everything we're talking about here is the body's aim to protect itself from an abundance of nutrition. Um, and so that's how I read this, is the body is doing... And specifically the liver, which is i- arguably the most important organ in this situation. And the liver's really trying to protect us, and it's saying, "I'm making so much extra fat right now because you as my individual are so far above your carbohydrate consumption tolerance, your, your tolerance for carbohydrate consumption. Um, and this is the most efficient thing I can do, which is turn that into fat, send it out via the VLDL, get that into the adipose site. And yeah, you're gonna be a little bit fatter, and it's gonna come with some downstream problems, but in the short term, it's protecting me, the liver." Uh, do you, would you agree with my teleologic view of that?

   12. SHSarah Hallberg1:00:14

       I 100% would agree with it. And again, you know, it, it's, I, I think that we're going to have more and more details on this coming out very s- very soon in many research product- projects that are currently ongoing.

7. 1:00:30 – 1:07:45

   The best early indicators of metabolic disease

   1. SHSarah Hallberg1:00:30

      But what it really comes down to is, you know, we wanna know what an individual's carbohydrate tolerance is. Okay? I mean, that's key to personalization, right? Does everybody need to be very low carbohydrate, low carbohydrate? I mean, where does... We can say population level, what happens in large clinical trials. But what's happening with the individual? Because let's face it, Peter, and, you know, you and I as practicing clinicians know this. When you're sitting with one patient in front of you, you can go over group data from a clinical trial, and that's important part of the decision-making, but the only thing that really matters is what's gonna happen with the patient right in front of you. We really wanna know what the individualized reaction is gonna be. You know, we know that this happens with a carbohydrate consumption above a certain threshold, but what that certain threshold is in the individual, we don't know. And based on these pathways, you know, what is the marker we wanna be looking at? Actually, it's probably POA. Surprisingly, not a fatty acid. But what this tells us is that when someone has consumed carbohydrates above their individual tolerance, that POA level is going to be a great biomarker. It's gonna go up as, again, a protective mechanism in the liver. Our livers are really-- I mean, you know, we talk about livers all the time, so related to insulin resistance. It's just always amazing just how sophisticated and how our livers, although we think of them as producing things that aren't necessarily good for us, and that may be true, they're also really working for us as well. Um, and so again, I wanna also go back on one other thing that you said. Um, and the other thing that you said is, so this comes, you know, before the adiposity. And I think that that is such an important point, and one I like to preach every opportunity I can get it. But this is starting to happen before people gain a lot of weight. Okay? This is a disease process in and of itself that causes obesity. So, you know, we have to really take that into account when we're in the office with someone who's struggling for, with obesity. And I know, Peter, you take this really to heart, of approaching and treating these patients without bias, um, a- and as I do. But it's, it's so important for other providers to be looking themselves in the mirror and asking themselves, you know, "What are the biases I hold, um, against patients who come to me struggling with their weight? Um, and what do I really know about the science?" And what it really one must conclude is that this is not their fault, okay? These are things that happened beforehand, and they're suffering the consequences of it, and the problem is the consequence is on full view for everyone to see. It's not something that they can hide, and that makes them so vulnerable to bias in healthcare. And again, one of the other things I come back to is part of our whole battle in health equity.

   2. PAPeter Attia1:04:12

      So Sarah, I wanna keep digging into this idea, 'cause it's so interesting to me, of having a leading indicator for, you know, this early, early, early warning sign. You know, I mean, I, uh, we talked about it at the outset of this discussion, which is, you know, in some ways the tragedy of using hemoglobin A1C as the marker of when somebody gets on the radar. I mean, you said it yourself. Patients will show up and nobody's ringing the bell until their hemoglobin A1C is above 6.5. But I mean, that literally is happening 10, 15, maybe 20 years after there were early, early molecular warning signs. And if measuring palmitoleic acid is one of them, uh, that's exactly the kinda stuff that I find interesting. Because in our practice, we use CGM a lot. So continuous glucose monitoring is kind of, you know-- We don't, you know-- Non-diabetics are wearing CGM like it's no tomorrow in our practice because of that exact reason. We're basically holding them to a very high standard of average glucose and high excursions and all these sorts of things. I wanna go back to something that you alluded to, which is the association between palmitic, palmitoleic acid and triglyceride is so tight that would we miss, for example, African American patients? Do we know if they are failing to synthesize C- C16:1 in the way a white patient is?

   3. SHSarah Hallberg1:05:39

      Wouldn't we love to know that? There's not been a good trial looking at that. I mean, one of the problems that we have in research in general is that we tend to focus on white people, right? Um, you know, and actually worse, middle or upper middle class white people. Um, so there are a lot of questions with this, um, in specific populations. Um, there have been a couple of studies recently coming out looking specifically at what we're talking about, POA, um, uh, and its marker for future problems and predictor of future diabetes and other issues. Um, one was a study recently published called the Panic Study, looking at levels in childhood and seeing how they translate to health consequences, you know, decades down the road. And then there was another study, I believe it was from the Netherlands, um, where they looked at POA levels at 50 to correlate them with C-reactive protein levels at age 70, right? And what we see is what we would expect based on our, our discussion here, which is the POA was a predictor of problems down the road in people who were healthy when their POA was elevated, or healthy so we thought. You know, what we really want to know ahead of time, and I know this is very meaningful to you in your practice, is I want the person who's healthy so I can get to, to tell them how to stay healthy. Okay? We, we talk a lot about, you know, trying to work on people who are already so, so to speak, behind the eight ball, and we want to work them out, and we want to regress their disease. Clearly an important goal. But we also really, if we're going to make a difference, again, with the individual and population-wide, we need to know who's headed for trouble.

   4. PAPeter Attia1:07:44

      Well, I mean,

8. 1:07:45 – 1:16:50

   Personalized management of metabolic illness

   1. PAPeter Attia1:07:45

      this is, a- again, I, I, I hope there's an ongoing effort here because I think this is the future of medicine, right? I mean, I think the, the future of medicine has to be coming up with tools that allow us to take broad, sweeping, you know, population-based insights and very quickly, uh, target individuals. And if we have biomarkers like this that can say, "Look, the moment this is triggered above a certain level, it doesn't really matter what your glucose is, and your insulin might still be normal, this is time to intervene." And then of course, the second part of that equation is what's the right intervention and how do we pair people to the right intervention? Um, and, and, and again, you and I have a very similar, um, set of experiences, which is, um, patients with hyperinsulinemia and elevated glucose generally respond well to carbohydrate restriction. Um, my practice also focuses so much on the role of glucose disposal and non-insulin dependent glucose disposal through exercise. Um, and I know that, um, you know, uh, that, that's probably not a surprise to many people is, is sort of correcting the sleep, exercise, nutrition trifecta, and then adding to that the, the role of cortisol in all of this. So I don't know. I, I think this is... I think this is a very hard problem to solve. That's the bad news. But I think the good news is if you get this one right, you get a leg up on every chronic disease. So-

   2. SHSarah Hallberg1:09:13

      Yeah

   3. PAPeter Attia1:09:13

      ... your risk of heart disease-

   4. SHSarah Hallberg1:09:14

      You do

   5. PAPeter Attia1:09:14

      ... cancer, Alzheimer’s disease all go down. Um, and, and so it's worth this enormous effort to, to continue pushing on these questions.

   6. SHSarah Hallberg1:09:26

      And I think, you know, on that note too, you know, and when we talk about individualization and risk prediction before we're seeing our classic, you know, biomarker issues come up, um, has to do... I'll, I'll, I'll circle it back to carbohydrate restriction because we know very low levels of carbohydrate restriction can, you know, reverse the disease process, m- uh, bring about normal glycemia, um, uh, in patients and be able to get them off of medications. But if we could put a risk predictor like POA into wider use, okay? Which would give a person their individual carbohydrate threshold, what if it didn't need to be as low? What if we caught them earlier in the disease process and we're like, "Hey, buddy, you go over, you know, 175, you know, that's where trouble comes in," rather than, you know, "You need to stay very low, um, you know, uh, indefinitely because we've caught you on the spectrum of the disease, you know, so late, and this is what we really need to do to control this to keep your glucose normal without the use of these many medications, especially insulin."

   7. PAPeter Attia1:10:42

      I want to ask you another question on this, Sarah. Um, and, and again, I don't know if it applies to patients that you've treated with diabetes or those in the prediabetes category, but have you, have you treated patients for long enough on ketogenic or very low carbohydrate diets who showed up in a state of metabolic disarray, ran through a lengthy period of this, so, you know, maybe spent years on a carbohydrate restricted protocol, and everything gets better. So they, they, you know, the weight goes along for the ride, but obviously, and more importantly, their metabolic markers improve, and they gradually reintroduce some amount of carbohydrate back in the diet, and all of a sudden they're fine, almost as though you reset them during a long enough period. Uh, how often do you see that, and what do you think is the best explanation for that?

   8. SHSarah Hallberg1:11:34

      See it all the time, and the best explanation for it is what is their insulin reserve? What is their insulin reserve? So, you know, the majority of people, um, can go ahead, you know, starting out even at long-standing diabetes, um, reverse their disease, get normal glycemia, um, get off of all their medications, um, and then slowly reintroduce carbohydrates as long as they have functioning beta cells. Okay? The problem is, you know, the longer you've had diabetes clearly is a risk factor for this, and we can... You know, w- we see evidence of that in the bariatric surgery literature as well. I mean, there's been so many studies looking at, um, uh, beta cells. Um, but, you know... And the fascinating thing is w- who is getting back some of their beta cell function, in other words, maybe their beta cells were only dormant and we're able to, you know, wake them up again, versus which are gone and not coming back. I mean, the fact that people were on the incredibly high dose of insulin, okay, starting on a very low carbohydrate diet, and then they got better right away, okay, uh, a lot of the change is swift, but they couldn't get off insulin, and it was just years went by, right? And they're just staying on this much lower level of insulin. And then all of a sudden they come off of it. I mean- We... Logic would tell us that some sort of beta cell function has returned. It took a long time. Reset the system, help them heal, you know? I mean, we don't completely understand this. There's so many great scientists looking at this right now, but we still don't have a certain answer, you know? 'Cause the answers w- on the personalized level is, how many of mine are dormant? How many of mine are dead, right?

   9. PAPeter Attia1:13:36

      Yeah.

   10. SHSarah Hallberg1:13:37

       What's it gonna take for me to wake these up, you know? If it's impossible, I'd like to know that because that sets expectations ahead of time, right? You can get a lot-

   11. PAPeter Attia1:13:47

       Right

   12. SHSarah Hallberg1:13:47

       ... better, but there's always gonna be a little insulin in your life. Um, it doesn't mean if they, um, uh, are someone who doesn't have any, um, insulin, uh, production capacity that they can't get a lot healthier, but they may not ever be able to get off of insulin. And so that's where it gets down, once again, into that nitty-gritty personalization aspect, and wouldn't that be nice to know? But I think that the answer to the larger question is, you know, why is this happening that some people can start to eat carbohydrates, uh, not anywhere near to where they were, but they're able to put some back into their diets versus people who can't, is, um, beta cell function.

   13. PAPeter Attia1:14:34

       Um, and I think something in there that you said is very important that I don't think, uh, historically has been communicated well enough to patients, which is that insulin, while an amazing and important hormone, is not benign, and there's a big difference between taking 100 units of insulin a day to achieve normal glycemia and taking 20 units of insulin a day to achieve normal glycemia. And you'll take the latter over the former all day, every day, non-negotiable. Um, and some patients will say, "Well, gosh, I'm still on insulin. This hasn't worked," and not realizing, no, you've had a five-fold reduction in your insulin requirement. That's an enormous improvement in your health outcome. Not... And, and let's put the economics aside. The economics are enormous, but ig- ignore that for a moment. Just in terms of health outcomes, uh, the, the negative effects of hyperinsulinemia. Um...

   14. SHSarah Hallberg1:15:24

       Yeah, and it... I just w- w- what want, want to say with that, you know, if we really think about the way we, we manage diabetes, okay, rather than work to actually reverse the disease process and get people off of medication, I mean, management constantly leads to more and more and more insulin, which we know... I mean, on the outward, the, the appearance of it, is that people gain more weight when they go on more insulin. But, you know, if we really get down to the nuts and bolts, when we take someone with Type 2 diabetes whose glucose is out of control to the point where we need to put them on insulin, the mandatory discussion that needs to occur is, "I'm gonna put this medica- I'm gonna give this medication, this insulin that you're gonna inject to you, okay? Um, and I'm gonna do that because your blood sugars are so high that they could acutely kill you, okay? Put you into the hospital, put you at risk of all these complications. But I just want you to know you're more likely to die on insulin." That's what we need to tell people. That's the truth. And, you know, that would have changed the approach a lot of patients want to take, and it would certainly... If, if, if providers were forced to look at it that way when they're staring each individual person in the face, maybe they would treat it differently as well.

   15. PAPeter Attia1:16:48

       Yeah. I, I,

9. 1:16:50 – 1:30:00

   Sarah’s cancer diagnosis and the beginning of her journey

   1. PAPeter Attia1:16:50

      I, I, I agree. Um, so I, I want to talk about, um, something that, that is, you know, uh, been such a big part of your life in the last few years, and people who don't know you may be almost surprised at where we're going in this discussion now. But, you know, this c- discussion could basically continue down the path if we could talk more about diabetes. We could end this discussion here, and, and pe- people would say, "Wow, that's a really insightful, uh, thoughtful person." But, but there's a whole other side, uh, to, to your experience with healthcare, Sarah, that started, uh, gosh, four year- almost four years ago. Um, and I'll tell it from just... I'll tell the beginning of the story just from my end. So you and I obviously, uh, met each other, uh, through Virta. You're, you're, you know, an early part of the, the creation of this, this company which is basically scaling up a way to remotely treat patients with Type 2 diabetes. Um, this is a company of, that, that Steve Phinney is also a co-founder of, along with Jeff Volek, I believe. Um, I have a minimal involvement in that company. I'm a small investor and, and at one point was an advisor. Uh, but it was during one of these advisory meetings that you and I happened to be sitting next to each other. Now, we'd met many times before that, but I do remember this very well. It was, I think, June of 2017. It was up in San Francisco, a large U-shaped, uh, table in the room, and, you know, it was a two-day ordeal. And, uh, you were sitting to my left, and that gave us more time than, than most times to be chatting about this, that, and the other thing. And, uh, you looked in perfect health as always. And, uh, at the end of the second day, I said goodbye and see you next time and blah, blah, blah, blah, blah. And then about a month later, I heard from a mutual friend that you had been diagnosed with lung cancer, um, and I just about fell off my chair. So can you tell people what happened that summer, the summer of 2017?

   2. SHSarah Hallberg1:18:51

      Yeah. So, you know, I'll just start by saying I, I've been someone who's taken taking care of themselves to, um, the max, you know, all my life. Eaten well. I've, I've kept my weight at a normal weight. You know, even nine months pregnant, I would have still been considered normal weight. Um, exercised like crazy, competed in, you know, half marathons, triathlons, Olympic distance, you know. I did everything right. Never smoked, you know. Um, never drank to excess. Um, and, you know, it was, it was June 30th, so right after that. It was June 30th of 2017. I was having a normal day. I was-- went to exercise. I had a big IRB meeting in the morning, went home, um, due to my wonderfully full house of three kids, and, uh, took a m- a business call in the basement 'cause that's was, that's always my escape place, you know, um, where it can be a little less noisy. And all of a sudden I couldn't talk. And I, I couldn't figure out what was going on. I knew something wasn't right, but, um, I, I couldn't speak. And, um, all I know is that I hung up the phone at some point 'cause I was embarrassed. I was-- remember thinking there, "He's gonna think I'm drunk." Um, and, uh, I hung up the phone and, you know, the next thing I remember was being in the car with my husband and him saying, "I don't think we could take you to urgent care." I have just very flashes of this day. And the next memory is in the trauma bay at the hospital, the hospital that I work at, um, where I had seen patients many, many times. And I'll have to tell you the other thing is the last time I had been in that particular trauma bay was when I brought my then four-year-old daughter in, or my husband did. I met them, um, via an ambulance after a traumatic brain injury. So it was like a very bad place for me, although my daughter completely recovered. And I remember s- screaming at my husband that, "They're wrong, they're wrong," and I wanted to see the computer because what had happened when they first came in is they thought it was a stroke, and so my poor husband was all of a sudden tasked with, you know, "Are you gonna give her clot-busting medication or not? Um, because we think she's having a stroke." But lo and behold, the imaging showed a really large tumor in my brain. Um, and, um, then they imaged the rest of me, and it turns out I had multiple tumors in my chest. Um, and so, you know, they presumed, you know, correctly at that point that this was lung cancer, but I also needed emergency brain surgery. And this is all, you know, I'm-- I, I, I remember most of this by people telling me about it. So, um, anyway, the next day I did, um, had urgent brain surgery. And then, you know, I, being a physician in lung cancer, you know, I was like, "That can't possibly be." You know, I have never smoked. You know, how do I have lung cancer? I am the healthiest person I know. I remember being in the hospital 'cause of course, you know, you're on drugs and everything else and, and of- and shock and everything, and I kept saying, "Look at my nails. These are the healthiest nails you've ever seen. How can this be a person who's sick?" 'Cause somehow that was like just one example, you know, of how that's impossible. Talk about the stages of grief and denial, right? And, um, being a physician and knowing what lung cancer meant, the next thing that came out of my mouth is, "I wanna move to Oregon," 'cause I was like, "I know what this means for me, and I know what this means for my family, and I, I don't wanna play any part in this. I don't want them suffering."

   3. PAPeter Attia1:23:02

      Can you tell folks what you mean by that? Not everybody might understand the implication of what you're saying.

   4. SHSarah Hallberg1:23:07

      Yeah. I wanted to go to Oregon because they had physician-assisted suicide. Because I, you know, I knew I have treated so many patients with lung cancer. I knew the horrible end. I knew what this meant. You know, um-

   5. PAPeter Attia1:23:24

      E- especially when it's spread.

   6. SHSarah Hallberg1:23:26

      Yeah, and it had spread everywhere. I mean, I had Stage Four lung cancer. You know, the day before I had been fine, 100% fine. That morning I had exercised vigorously. And suddenly I'm in the hospital recovering from a brain surgery, being told that I have a rapidly fatal disease. And, you know, all you can think of in that ma- moment of panic is your family, right? And so, you know, my only thought was, "I, I don't wanna watch-- I don't want them to watch me go. I want them to remember Mom." And so, I mean, there began my, so far, almost four-year journey of a new me. You know? I-- Cancer changes you, so I'm not that person, you know? And, and one of the many things is sometimes at this point in time, you know, I mourn that person.

   7. PAPeter Attia1:24:31

      I mean, one of the things that I think is very shocking for people to understand is that probably between 12 to 14% of people who get lung cancer are not smokers. Um, and they all tend to get a certain type of lung cancer. You know, lung cancer is broadly divided histologically by small cell and large cell, or non-small cell, I'm sorry, and within the non-small cell there's large cell, adenocarcinoma, squamous cell. And most of the people like you who are not smokers get this type of adenocarcinoma non-small cell, and it is really shocking to think that given the prevalence of lung cancer and the lethality of lung cancer, lung cancer kills more people than any other cancer, um, and I believe that's true for male and female still. Um, to think that-

   8. SHSarah Hallberg1:25:21

      Yes. I mean, by far

   9. PAPeter Attia1:25:22

      ... yeah, to think that such a high percentage, 12 to 14%, could be non-smokers, uh, tells us this, the severity of this. Um- I also think it's worth reiterating something you've said, which is sort of the miracle of the fact that we're sitting here having this discussion four years later. The, uh, median survival, meaning if you took, you know, 100 people, um, with stage four, which means a type of cancer that has spread from its original site of origin, and in your case it went to your brain, which is a particularly devastating place for this cancer to grow, the median survival of people with stage four lung cancer is probably 12 months or less, correct?

   10. SHSarah Hallberg1:26:07

       Well, it depends on what kind of lung cancer that you have. But yeah, I mean, um, and sometimes even eight months or less. Um, and, um, those were the stats that I knew when I was first diagnosed. And, you know, one of the things that I'll say is non-smoking lung cancer is growing at scary rates. It's being diagnosed, and it hits people in their prime. It's growing rapidly, especially in young women, so it's hitting a lot of moms. Um, much more common in women than it is in men, although it does happen in men. Happens in Caucasian and Asian women predominantly. And the interesting thing is most of the people that it impacts are thin and in shape or athletes.

   11. PAPeter Attia1:27:04

       Do we have any insight into why?

   12. SHSarah Hallberg1:27:08

       No. And, and it's one of the things that's not being investigated as much, you know? When you look at, okay, you know, w- what studies have been out there, oh, we get the typical, you know, it's radon, it's, you know, um, uh, uh, you know, being next to a smoker. I never was, okay? My father was a smoker. He quit smoking the day I was born and never went back. I was not raised around smoke. Um, so, you know, you... The fact of who it's impacting and, and the fact that the, the demographics of the people that it's impacting are the healthy people. You know? W- unlike what we associate with, you know, our epidemic of insulin resistance, that's not who these people are. We know that insulin resistance is responsible for a huge number of cancers and, and, and cancer rises. That's not this, you know? And so, you know, it's, it's young women, um, and, uh, again, who have presumably done everything right. Um, a- and it's just, it's something that is not getting enough press. I know The Guardian did a big story about it about a year ago. Um, but otherwise it's not getting the attention it deserves. And these women really wind up, um, with two different kinds of cancer. They wind up with EGFR-driven cancer, that's epidermal growth factor receptor, or they wind up with something called ALK-positive cancer. I have the EGFR, specifically something called EGFR exon 19 mutation. And the thing I didn't know at diagnosis because, again, I had been focused on obesity and metabolic disease and diabetes for so long, um, you know, I hadn't been seeing as many people with active cancer as I did when I was in primary care. Um, and so I was quite frankly behind, um, on some of the newer treatments and newer, um, diagnoses, if you will, and we're talking the genomics, um, of cancer. Um, but for EGFR cancer, there was something called a targeted therapy. This class of medications is called tyrosine kinase inhibitors. And, you know, people can go on them, and they can get better, okay? They can even, in many cases, have all of the cancer go away, okay? Doesn't mean they're cured, though, because it always comes back. And so after initially, you know, again,

10. 1:30:00 – 1:40:30

    The emotional impact of a devastating diagnosis

    1. SHSarah Hallberg1:30:00

       going through all these... I mean, I'll tell you, the, the denial grief stage.

    2. PAPeter Attia1:30:04

       Well, I, I wanna, I wanna actually ask you exactly about that, Sarah. Uh, I wanna go back to what is it like when you were recovering in the hospital from the brain surgery? Because I assume they had not taken out the primary tumors in your lungs. They were just alleviating the most life-threatening symptom you had at the moment, which was a mass inside a part of your body that can't accommodate a mass, which is why you had a seizure. Um, so they take that out. You're recovering from a surgery that by itself is difficult to recover from. But then coupled with the knowledge of, "Here's this disease, and my lungs are full of this." I... W- what do you remember of those days?

    3. SHSarah Hallberg1:30:47

       Overwhelming grief to the point of not being able to think. And again, it's, it's... You know, of course, I come and approach everything in life as a mother, right? I mean, and, and, and I'm not saying as a mother only, like, fathers would do the same thing, but you approach every problem in life through what it means for your children.

    4. PAPeter Attia1:31:10

       How, how old were your children at the time, Sarah?

    5. SHSarah Hallberg1:31:14

       They were seven, 12, and 14, and they needed me. They still need me. Um, and so the grief is overwhelming about... What I quickly realized is I'm gonna break my children's heart, and there's not a thing I can do about it. And to have that realization, 'cause it comes quick, and have to sit with that, is a grief I can't, I can't even explain. And so I mean, initially I just was... I couldn't handle the grief. I h- I had to be denial, in denial. I came home from the hospital, I had just been discharged from ICU, and I walked seven miles the day I got home. And my feet were... See? I c- I can't be sick. I, I, I just got out of this brain surgery. I'm still on medication. I walked seven miles today. I'm healthy. I don't know what you people are talking about.

    6. PAPeter Attia1:32:27

       What did your kids know at this time? Had your husband already spoken with them?

    7. SHSarah Hallberg1:32:31

       Well, sadly enough, and I actually didn't find this out until quite a bit later, they are the ones who found me in the basement. So, you know, talk about not telling the children. We had... That was never an option for us. So, you know, they knew I was having surgery, that there was a tumor in my brain and that this was cancer. This is not good. Um, and that's a lot for a kid to unpack, right? Especially a kid, you know, again, I mean, it's, it's hard for any kid to unpack, but, you know, one of the things I remember when my kids were going through each of their own... Every one kid goes through it, the phase of, "What if something happens to you, Mommy? What if hap- something happens to you, Daddy," right? All kids go through that, and the one thing, we used to kinda laugh together, my husband and I, about that. Say, "Oh, honey. Your mommy and daddy are the healthiest people."

    8. PAPeter Attia1:33:40

       Hmm.

    9. SHSarah Hallberg1:33:41

       Um, "We are so healthy, you know, you don't need to worry about that." And, and I remember that. You know, it's one of the, one of the first things that you think of when you're put in this situation is, "Oh, my God." You know, they have to unpack this in that context. And it's hard to be a teen. It's hard to be a seven-year-old. But to be one whose mother suddenly had a, you know, diagnosis of advanced cancer... And we, it was a l- hard decision on what to do, but, you know, in talking and how do we handle the kids, but the one thing we decided together, me and my husband and I, um, is that we were never gonna lie to them. You know, we were always gonna tell them the truth, because I thought that the worst thing for a kid is to constantly be wondering if something, if there's gonna be a huge shoe that drops. And so w- we told them. We tried to open up the lines of communication. They mostly didn't wanna talk about it. Um, but we told them that we were making that promise to them, and we have never, never gone back on that problem, and promise and never will. I, I mean, that's one that it's really important to me. We may delay telling them something for a little bit until we really know the facts, but as soon as we really know the facts, they're gonna hear about it. So, um, anyway, I mean, you know, and over time, in grief you learn to accept many things, you know? My husband and I, our dream had been to, um, retire to a farm and make, um, gourmet butter.

    10. PAPeter Attia1:35:36

        Hmm.

    11. SHSarah Hallberg1:35:36

        Like, that's what we were gonna do. That was gonna be the second career, right? And you learn to make peace with that's not the case anymore. You know, our, our... We always used to joke that the way we wanted to die was w- 95 years old on the way home from a skiing trip-

    12. PAPeter Attia1:35:54

        [laughs]

    13. SHSarah Hallberg1:35:55

        ... in a fiery car accident where our kids would not have to deal with the bodies, right?

    14. PAPeter Attia1:36:01

        The cremation, the twofer one.

    15. SHSarah Hallberg1:36:01

        But we wanted to make sure it was on the way home.

    16. PAPeter Attia1:36:03

        Yeah.

    17. SHSarah Hallberg1:36:04

        A twofer. It was gonna be on the way home, because we were gonna be having fun up until that point. Um, and, um, you know, you d- so that's acceptance, you know? You're not gonna retire. You're not gonna have all these things. But you can't accept that you're not gonna be a mom. Impossible.

    18. PAPeter Attia1:36:30

        Now, at some point, I'm guessing kinda the problem solver in you started saying like, "Hey, I, I'm gonna learn m- as much as can be known about this." Um, and we're gonna talk about this in the context of the asymmetry that exists. Um, I, I just had a discussion about this with... You know, we have a weekly meeting in our practice with all the providers and, you know, we just had this weird situation recently where, y- you know, basically a, a patient of ours who has another physician, uh, was kind of caught in the middle of a recommendation that turned out not to be the right recommendation and, you know, we were able to get them a referral to somebody else who basically got them out of a very unnecessary surgery. And, uh, we were just sort of thinking, "Man," like, "we're so glad that that patient was able to dodge that bullet," you know? They were gonna have, uh, a surgery that they totally didn't need, um, that's a very big surgery with lots of risks, and we realized like the asymmetry of knowledge in medicine is so overwhelming that it is It, it, it's, it's, it's not even just about money or education outside of medicine. Like, a, a smart person still has a hard time digesting medical literature. Um, and I know, like I said, we're gonna talk about this, but I, I... You know, you very quickly must have figured out, hey, I have this EGFR, uh, 19 deletion. So we no longer talk about this as you have lung cancer or you have adeno or you have non-small cell. We're really gonna refer to it by its mutation, and everything will come down to how do we treat that. How long was that process for you to say, "I'm gonna..." I don't know if there, this is the right word, but, "I'm gonna partition my grief and my problem-solving brains, and I'll pr- I'll do both of them, but I'll, I'll, you know, I'll, I'll move back and forth"?

    19. SHSarah Hallberg1:38:35

        Pretty quick. It happened pretty quick. Um, which is, okay, you know, this is terminal, right? You have to come to, to grasp at that, but terminal when, right? And what can I do to control the when?

    20. PAPeter Attia1:38:55

        But when you say that, Sarah, did you really come to that realization so soon? Because technically, life is terminal. I mean, there's nobody listening to this podcast, watching this video, who isn't gonna die, so that's all terminal. But when you say that, do you mean that immediately and without question or reservation you felt that you would not live a normal life expectancy? There was no Hail Mary out there that was gonna, you know, take you to being the 95-year-old skier?

    21. SHSarah Hallberg1:39:26

        Um, yeah. I mean, I th- I think just the reading and understanding, although the advances, that, that this was gonna be terminal really soon, you know, in my life, and I was only 46 at the time. And, you know, my first thing was just please let me make it to 50. I'm 49.

    22. PAPeter Attia1:39:50

        You're gonna be 50 soon.

    23. SHSarah Hallberg1:39:52

        Yeah, I'm gonna be 50, um, in the not too distant future. So, you know, that was, like, my first one was just like, okay, let's, let's... But right from the beginning, I'll tell you, the when was 11 years, okay? And, and that has not left. I just, I don't need to re- be 95. I can accept all those things that I'm gonna miss out on by not growing old. I just need 11 years, which to everyone was unrealistic. But why 11 years? Because my youngest would be graduated. Uh, so, so

11. 1:40:30 – 1:52:15

    Sarah’s plan to extend survival

    1. SHSarah Hallberg1:40:30

       immediately my goal was I can't settle for less than 11 years. I have to make it to 11 years. And so it became that, like, my war cry, 11 years. 11 years. I have to make it 11 years. And so, you know, it started... I mean, and, and that started me on a path of so much. So the first thing I thought in reading all the... I mean, read everything, is I gotta get this primary tumor out. You know, I'm considered inoperable, but we know that having this primary tumor here increases my risk for mutations, okay? Remember I said that the tyrosine kinase inhibitors, or the TKIs, they work amazingly well, but only so long. You know, somewhere between eight and say, you know, on average eight, and with the more, um, advanced ones, you know, at the long end is, like, you know, 24 to 30 months, okay? Um, so that's not enough time. That doesn't get me to 11. [laughs] So I was like, okay, you know, this is increasing the risk for mutation, which is how these develop, um, resistance to the tyrosine kinase inhibitors.

    2. PAPeter Attia1:41:45

       And, and remind me, Sarah, you, um... 'Cause I remember you emailing me probably by August and, and starting to, you know, explain some of the details. You ha- Your biggest tumor was, like, five centimeters. That's a monster tumor. How-

    3. SHSarah Hallberg1:42:00

       Huge

    4. PAPeter Attia1:42:00

       ... how many tumors did you have?

    5. SHSarah Hallberg1:42:01

       Six.

    6. PAPeter Attia1:42:01

       It was six centimeters, or you had six tumors?

    7. SHSarah Hallberg1:42:05

       I had s- It was six centimeters.

    8. PAPeter Attia1:42:06

       Wow.

    9. SHSarah Hallberg1:42:07

       Mm-hmm. Which is amazing in the sense that I never had pain from it. You know, it never, I never had a cough.

    10. PAPeter Attia1:42:15

        Probably because you were so healthy. [laughs]

    11. SHSarah Hallberg1:42:17

        I think so, because, you know, I, it... This talk about being caught out of the blue, you know, there just wasn't this premonition of something is awry and I'm just not addressing it. Um-

    12. PAPeter Attia1:42:27

        And so the standard of care, sor- sorry to interrupt, was just that, you know, we typically don't operate on patients with metastatic tumors. It's, it doesn't... The only reason they operated on your brain was it was an acute way to save your life. I think, uh, it's hard for patients listening to this to understand that, but that's sort of the, that's the playbook in oncology, right? When a patient shows up with metastatic cancer, they're considered not surgical candidates, and this was the exception and not the rule. You were gonna be dead probably within days if they didn't operate on your brain. But all this time afterwards, you still have these, this burden of tumors in your lung, and now the question is, can we improve your prognosis? And maybe that doesn't mean you live to 95, but can we reduce, can we make your cancer less resistant to therapy by taking the majority of the cancer cells out of your body?

    13. SHSarah Hallberg1:43:24

        Right. You know, um, and, and decreasing the tumor burden, because really quickly the TKI got rid of every single small tumor. I had them throughout, you know, like, paint splatters on, throughout both lungs, and they were gone in a matter of weeks.

    14. PAPeter Attia1:43:42

        That's staggering, isn't it?

    15. SHSarah Hallberg1:43:44

        I mean, it is. It's, it's remarkable, but the, you know, again, the primary tumor was huge, so, um, I had unfortunately the large tumor in my brain was not the only one. I had two other ones that they radiated. Um, they didn't need to be surgically removed. They were small. They could be radiated. And then I set about trying to find someone who would take out this primary tumor. Um-

    16. PAPeter Attia1:44:11

        Can I, can I ask you about the stereotactic radiation, Sarah? That's-

    17. SHSarah Hallberg1:44:14

        Mm-hmm

    18. PAPeter Attia1:44:14

        ... I mean, we glossed over that, but that's not a benign process either. Did you suffer nausea from that? What... How difficult was your stereotactic treatment? Did you take it all in stride?

    19. SHSarah Hallberg1:44:27

        I did great with the treatment to the brain. I didn't have any issues. You know, I did have issues at the beginning, but they were more to the TKI. You know, one of the things with every specialist that I saw, you know, they couldn't believe it, or they told me, "If I saw them earlier, it wasn't gonna happen. You know, at least you'll keep your hair." All my hair fell out. Like, it wasn't supposed to happen. Like, your hair is not supposed to fall out with TKIs. All my hair fell out. Anyway, so the brain radiation went fine. Um, and then I met a surgeon who was going to take out the primary tumor for the reasons that I was saying. We just... Anything to decrease the risk of, you know, um, uh, developing a mutation that keeps me from being sensitive to the TKIs. And so I went in, you know, for surgery in September, and I can remember her saying, "We're gonna take this tumor out. We're gonna take out your right upper lobe, unless, of course, we've seen that there's disease in the mediastinum." But there was no disease on the PET scan in the mediastinum, so she was feeling pretty positive about being able to take that out. But I knew for several weeks beforehand that that was a possibility.

    20. PAPeter Attia1:45:51

        And just so folks know what we're saying, on the, on the right-hand side, you've got these three lobes here, but they drain into these lymph nodes that are in this middle structure called the mediastinum. And so you had this monster tumor that was gonna require the entire upper right lobe to be taken out, but if the surgeon felt that on visual inspection, at least, or maybe even sampling nodes, that any of those nodes had cancer, it was her opinion that this is really futile because now we know it's already escaped the lung. It doesn't matter. So, so you went into that surgery knowing you could wake up with a huge scar in your chest, chest tubes coming out, and the cancer is still in you, right?

    21. SHSarah Hallberg1:46:38

        And that happened. Um, and that was... I, I mean, it was terrible. I mean, you know, uh, uh, I kept apparently, you know, under the influence, I, I mean, everyone told me... I was so hysterical screaming in the recovery room, "I'm a mom. You can't let this happen to me. I'm a mom." That's all I kept saying, and I, of course, don't remember any of this. But they had to actually take me away, put me in a private room, and, and that was all that I kept saying. And, um, so, you know, I had to come home and, and learn to accept that. Um, I now was bald, and, um, I was definitely fell into a deep depression, but at the same time, you know, I refused to completely give up. I mean, like, for example, I went back to work at the clinic the same month that I had brain surgery, you know, which sounds crazy. But this is part of this whole process, and then... But after the surgery failure, I, I mean, I was... It was... That was terrible. Um, and then I didn't really recover back into my determined place until a really very specific moment, and that was just a couple of weeks before my diagnosis. Um, I had been selected to be an Aspen Health Innovator Fellow, which was... I mean, this is among the higher, highest honors for your work. You know, this is... The Aspen Institute is, you know, a place that brings together thinkers in all kinds of disciplines and, you know, to be chosen to represent people who are innovating in the healthcare space was, I mean, such an honor. And in order to do that, you had to commit to four weeks of leadership sessions in the next two years, which of course at the time I was like, "Of course, sign me up." But as that first session inched closer, it was in November, I, I was so, "What do I do?" I couldn't make up my mind. I literally didn't make up my mind for sure until I sat-- I got on the airplane, and because I was ready to run back. Because it was like, "I'm gonna leave my kids for almost a week? I have terminal cancer?" And at that point, I decided you can live feeling sorry for yourself and of all the things that you're gonna lose, or you can go out and live, and your kids are gonna be better for it. This is what really made me decide. Your kids are gonna be better if you choose to live. And so that was the moment, sitting on that plane seat. Crying. Never cl- I've cried on a lot of planes since [laughs] this diagnosis, deciding I just chose to live. This was a moment. I made my choice, now I gotta stick with it. And that's how I've tried to live my life since then because I, you know, I have a platform, I had a platform. I had done what I feel was a lot of good for a lot of people and it wasn't finished, and I knew that this was good for my children, and I'll tell you one of the most impactful moments of my whole life happened before my diagnosis. And it was one of these times where we were at the dinner table and the lottery happened to be one of those, you know, hyperinflated lotteries. Oh my God, you can win, you know, bajillion dollars. And so my husband and I were at the l- dinner table joking around about it, right? I mean, we don't play the lottery, but we were joking around, "Maybe we should buy tickets," you know? "We could retire. We could retire." And here at the time was my 13-year-old son at the dinner table, and he got really upset about us discussing this. "You can't retire, Mom. You're doing so much good for the world. How could you even think of it?" I've never been so... That is a defining moment of my life. And, and, and like, I, I was like, oh my God. You know, at the time I just... I was so taken aback by that. And, um, certainly that weighed heavily on my decision to get on that plane and to continue doing what I'm doing. Um, and what I'm doing has morphed since my cancer diagnosis into an even greater focus on health equity because of my experience as a cancer patient and someone who is privileged. Because I'll tell you, you have a much greater chance of surviving cancer if you are a... has privilege, uh, you know, one of the lucky ones, and I didn't realize the stark differences until I became a patient.

12. 1:52:15 – 2:05:00

    Sarah’s aggressive treatment plan

    1. PAPeter Attia1:52:16

       I wanna talk about that in some detail, Sarah, but I, I wanna also understand how it is that we're still talking today, frankly. In other words, how have you managed to, um, stay in an equilibrium with this disease? Right? I've always... I mean, let me, let me [laughs] share with you a couple of things that I, I, I've always struggled with when thinking about cancer. I, I'm not fond of the language that we sometimes use around cancer, and that we beat cancer and that, you know, we can't give up and things like that, uh, al- because it almost suggests that the patients who don't survive cancer have somehow given up, and I, I just, I, I, I just don't find that, in my experience, uh, having taken care of many patients with cancer, to be true. I think, um, I just... You know, it doesn't make sense to me. Um, and I think the way that you said it and described it earlier makes the most sense, which is basically finding a way to coexist with your cancer for as long as possible. Um, and you've exceeded all odds. A- a- and I, I wanna kind of understand that journey a little bit more. Um, y- you know, uh, it's, it's one thing to, to go through the tyrosine kinase inhibitor, have this immediate response, um, that's remarkable, but then get this setback, you know, three months later where your primary is not only still there, but you actually realize now there's, there's mediastinal involvement, um, which basically means there's no question you have cancer cells elsewhere in your body. Um, it's not like they stop when they get to the lymph nodes. So pick the story up for us in terms of what your ongoing treatment has been life- like. How have you stayed in this, in this state of, uh, of equilibrium, so to speak?

    2. SHSarah Hallberg1:54:10

       Yeah. S- so I haven't, okay? Um, on many occasions I haven't. Um, uh, but so, so after the surgery, um, the next thing that happened is they found another brain tumor. Um, there's argument as to whether it was there from the get-go or, um, uh, whether, um, it was something new. Um, but either way, they decided it would be considered, um, that the first line TKI that they had put me on, um, had failed me. Um, and so I got switched to... I got more radiation to the brain, and I was switched to, um, an- the newest TKI. Happens to be called osimertnib or Tagrisso. I was put on that in November, um, right before I went off for my first Aspen Leadership Conference. Um, and I had decided that I do not accept being a sitting duck because what the cancer world then, you know, wants is for a patient like me to just sit and wait for the cancer to come back, right? That's what you're doing. You know it's coming back. There's no question about it, and you know it's coming back soon, and, you know, you are just waiting, and I couldn't accept that as a mother I think I could accept it as a human, but I couldn't accept it as a mother. And so I went on a journey to find someone who could treat me in the most aggressive way possible, who shared my view that sitting around and waiting for this to come back was totally unacceptable. I traveled the country. I saw everybody, let me tell you. First of all, of course, that shows I have means to do that, right, that a lot of other people don't. And I actually, along the way, met another mother, physician, my age, just a bit younger, younger kids, who had the same attitude towards it, "I w- refuse to accept this." We sort of became a team, so to speak, and wound up, by complete serendipity, meeting a group of physicians who really felt that the way to treat this long-term was to be constantly battling it with something new. So in other words, you know, the, the cancer dogma right now is you put people on something at the highest dose possible, and you keep going until it doesn't work anymore. That, that's how we deal with cancer. And then we switch, and it's the same thing over again. And the idea is what if we hit it with less and then change it up all the time, right? And this goes to the idea of beating the mutations before they can get you. So thankfully, I had a physician here at home who was willing to say, "Okay, that, that is worth a shot." February of 2018... 2019, okay, 'cause it took a long time to get to this point, right, of searching, trying to find something. I started chemo, um, regular chemo. I went through the regular cycles of chemo. And then when I was done with that, I immediately went to anti-estrogen therapy, okay? 'Cause I had a very specific mutation besides the EGFR one, and there was a medication to treat it. It just so happened to be a breast cancer medication, but it was the same mutation for either cancer. So immediately upon stopping, um, the chemo, I went on the anti-estrogen therapy. So I was put into early menopause with a number of, you know, regular medications, Lupron, Fulvestrant, and then I was started on a medication called Palbociclib, okay? Which, again, is primarily a breast cancer medication but was targeting one of my very specific secondary mutations. I was on that for the summer, and all this time I'm still on the Tagrisso or osimertinib. That never stopped. As soon as the eight weeks of that was over with, I went back on chemo, but very different. Low-dose chemo. Um, single agent, very low dose.

    3. PAPeter Attia1:59:24

       Which agent?

    4. SHSarah Hallberg1:59:25

       So the first one was cisplatin.

    5. PAPeter Attia1:59:27

       Ugh.

    6. SHSarah Hallberg1:59:29

       Okay. And, you know, everyone says, "Oh, cisplatin, you know, you're, you know, you're gonna do terrible on this. I mean, this is harsh." It, and it is. But, you know, I did fine. I did fine. I was able to still, you know... I mean, I'm not saying I wasn't tired. You know, I've basically been nauseous for the last f- almost four years, every single day, you know? It's just you learn to manage that, you know. So I learned to manage it. I learned to manage, you know, being tired, um, and the things that came along. I still traveled for work. I still did, I was still able to do everything. Um, I just, I can't imagine, I can't... Like, I, I could tell you some really crazy stories of, of things I had to do while traveling to accommodate how I was feeling, um, that nobody knew about at the time.

    7. PAPeter Attia2:00:18

       [laughs]

    8. SHSarah Hallberg2:00:19

       But anyway, um, some really wacky stuff that you do, but you just, you manage. You, you figure it out, right? You improvise. Lots of improvising. Um, and then, um, I got switched to an- another, after eight weeks, got switched to gemcitabine or Gemzar.

    9. PAPeter Attia2:00:39

       Which again, these are so cra- You just don't think of this because that's a drug that's typically used in pancreatic cancer, right?

    10. SHSarah Hallberg2:00:47

        Well, yeah, and it can be used in lung cancer too, and, and of course-

    11. PAPeter Attia2:00:49

        I mean, it just depends on the mutation. I think that's the point, right?

    12. SHSarah Hallberg2:00:52

        Right, right, right. Yeah. Um, th- believe it or not, there's no standard chemo for lung cancer. It's... Can you believe that? There's not a standard, like, k- standard of care regimen. So the thing is I wasn't doing any outlandish things here. Okay? These are all treatments for lung cancer. Okay? I mean, uh, like y- like you said, Gemzar is used more for other things, but this is not an outlandish thing that's never heard of for lung cancer. I mean, same with cisplatin. I mean, um, none of these things are, you know... Uh, uh, it, it, you know, I was, "Oh, my goodness, we're gonna, you know, do something, you know, that's never, ever been done before," you know, so to speak, things. These are just-

    13. PAPeter Attia2:01:30

        And, and at this point, which is now the fall of 2019, where... If, if you go and get a PET scan, where do you actually have tumor in your body at this point?

    14. SHSarah Hallberg2:01:42

        So yeah, let me back up for a second because... Well, the quick answer is I had no tumor.

    15. PAPeter Attia2:01:48

        Okay.

    16. SHSarah Hallberg2:01:48

        There was no tumor anywhere. And to back up is that the Tagrisso, this is pre-chemo Had stopped shrinking my primary tumor in March of 2018. So this was, you know, almost a year before I began chemo. And so since they wouldn't surgically operate it to get it out, I had it radiated. Again, you know, I was lucky enough to have a radiation oncologist who worked with me, and, um, and like I said, I, I tolerated brain chemo well. The same was not the case-

    17. PAPeter Attia2:02:29

        Brain radiation

    18. SHSarah Hallberg2:02:30

        ... for lung, t- to the lung.

    19. PAPeter Attia2:02:33

        Yeah, the radiation.

    20. SHSarah Hallberg2:02:35

        I had real issues. Um, and interestingly enough, you know, we were leaving for, to hike the Inca Trail in May of that year. So I had had radiation, then we were leaving to hike the Inca Trail, and I started having kind of bad chest pain. It was like w- like a day or two before we hiked the Inca Trail. I was like, "Okay, I'm sure this is just reflux. I'm gonna take some reflux medication." And then I was like, "Look, okay, if it's not, if it's more, you know, what a better place to die than surrounded by your family, you know, on the Inca Trail and all the beauties of the Andes Mountains? Okay, I can accept this. Let's go." You know, I didn't even tell anyone. I was like, "Going forward," and, um, did that successfully, you know? Um, it was great. My eight-year-old toodling along. You know, she was always the fastest of any of us. We went with our friends and, um, uh, I mean, a- a- amazing experience. I just have to say that those things, especially if you can get kids in it, I'll never forget that when we all got back and we went and checked into the JW because we were like, "Give me a shower, a very clean bed, and a spa," my middle child, my daughter, said to all of the adults, "I developed my third eye during that."

    21. PAPeter Attia2:03:59

        Hmm.

    22. SHSarah Hallberg2:04:01

        It was one of those experiences.

    23. PAPeter Attia2:04:02

        Wow.

    24. SHSarah Hallberg2:04:02

        Like, you don't normally think you're gonna get that out of a... You know, she was, what, 14 at the time. You know, that's, that... We were all like, "What?" [laughs]

    25. PAPeter Attia2:04:12

        [laughs]

    26. SHSarah Hallberg2:04:13

        But anyway, so it was a super special time. I was still having pain, and then my rest of my family flew home. I actually had to fly, um, from Lisbon to Switzerland because I had a conference I had to go to, and at that conference, things started to get really bad. Um, I made it through, but, you know, not with, again, some funny stories of, of how I accommodated to it, 'cause I was having crushing pain. Got home, s- turns out, of course, I had some rare, I had this rare complication where it actually impacted my bones, and my radiation oncologist said, "The only treatment for this is to put you on long-term opioid therapy."

    27. PAPeter Attia2:04:56

        Oh.

    28. SHSarah Hallberg2:04:56

        And I was like, "Uh, no, thanks. I will accommodate." [laughs] There was

13. 2:05:00 – 2:18:26

    Life-threatening complications and the return of her cancer

    1. SHSarah Hallberg2:05:00

       no way I was doing that. So I had to get through that, which was a, which that was a little bit of a saga. But anyway, I had no disease then after that radiation, none. And so I was in this state, they call it NAD or NED, excuse me, no evidence of disease. I like to always say NED, right? Had n- I was NED for a really long time. I had no evidence of disease. It was a great place to be, right? Still on treatment, still trying to do everything to keep this from coming back, and started Gemzar. And, you know, everybody had said all these terrible things about cisplatin, and Gemzar was 10 times worse. Everyone was like, "You'll, it'll be a breeze. Gemzar is a breeze compared to cisplatin."

    2. PAPeter Attia2:05:42

       You, you are really the exact opposite of everybody, 'cause yeah, I mean, we used to tell patients-

    3. SHSarah Hallberg2:05:47

       I, I, yeah

    4. PAPeter Attia2:05:47

       ... Gemzar is, it's non-chemo.

    5. SHSarah Hallberg2:05:51

       Yeah.

    6. PAPeter Attia2:05:51

       [laughs]

    7. SHSarah Hallberg2:05:52

       Yeah, e- everybody tolerates Gemzar. I can still remember sitting, 'cause I was too, feeling too crappy to drive, my mother driving to pick me up to take me to chemo one day, sitting on my front porch and throwing up in a plant on the way to chemo.

    8. PAPeter Attia2:06:07

       Uh, there are nutrients in there, Sarah, that are very good for the plant, so I wouldn't, I wouldn't-

    9. SHSarah Hallberg2:06:11

       That's right

    10. PAPeter Attia2:06:11

        ... feel bad about that. That's very, it's a very healthy part of the carbon cycle, I'm sure.

    11. SHSarah Hallberg2:06:16

        But I was determined to, you know, keep on. I was really close to getting switched to Taxol, which, you know, I'm like, "This is gonna ha- that'll be better." Um, and, um, so then had to take another trip, um, for another meeting and had lots of friends there, and I can remember them standing behind me after we had eaten, and they were pushing me up this hill in San Francisco 'cause I literally couldn't walk. And I kept thinking to myself, "I'm a hypochondriac. This is just because I'm anemic," you know, whatever. Um, I was super short of breath. Um, but I'm like, "Okay." I, I had convinced myself I was making it all up in my mind. I fly back from that trip, and the very next morning, head in for chemo, and they immediately said, "Oh my God, no chemo. You know, everything is a mess." My, I... You know, my liver numbers were through the roof. My kidney numbers were, you know, high. Um, I had pancytopenia so bad, um-

    12. PAPeter Attia2:07:27

        How, how anemic were you, Sarah?

    13. SHSarah Hallberg2:07:29

        So I was, like, six at this point, okay? I mean, it was bad. It, you know, really bad, the low sixes at this point.

    14. PAPeter Attia2:07:36

        Right, and just so the listener understands, yeah, the, the, the normal would be 13 or 14 of hemoglobin, and you're six, so that's really low.

    15. SHSarah Hallberg2:07:44

        I'm bad.

    16. PAPeter Attia2:07:44

        And your platelets were how low?

    17. SHSarah Hallberg2:07:47

        23.

    18. PAPeter Attia2:07:48

        Which means you basically don't have the ability to form a single clot.

    19. SHSarah Hallberg2:07:53

        Right. Uh, you know, I was a disaster. And the funny thing is I was still up and doing okay. You know what I mean? I was tired. I was shortness of breath with activity, but I was doing okay. And they sent me home. And I was like, "Uh, uh, uh, that doesn't seem right. Am I crazy that I shouldn't be home?" So of course, I call some of my other physician friends. Aha, privilege, right? 'Cause I was getting sent home.

    20. PAPeter Attia2:08:24

        Mm-hmm.

    21. SHSarah Hallberg2:08:26

        And they're like, "Oh my God, we're admitting you right now." Right? So I actually get a backdoor admission to the hospital and a complete workup starting right then. You know, I had to be... I had to have a thoracentesis, drained a whole bunch from my lungs. That was unknown when I got sent home.

    22. PAPeter Attia2:08:50

        So you had tons of fluid-

    23. SHSarah Hallberg2:08:51

        Kidney failure

    24. PAPeter Attia2:08:51

        ... around your lungs. That's obviously explaining-

    25. SHSarah Hallberg2:08:54

        Tons of fluid around my lungs

    26. PAPeter Attia2:08:55

        ... the shortness of breath.

    27. SHSarah Hallberg2:08:57

        Yeah. Um, and once I was admitted, I was promptly transferred to ICU. Things were going downhill. I had to be put on BiPAP, so I had multi-organ failure. I, you know, had respiratory failure, liver failure, kidney failure. I was a big failure, okay? Everything was bad.

    28. PAPeter Attia2:09:16

        And was this believed to be the result of, uh, your body's response to the tumor or the chemo?

    29. SHSarah Hallberg2:09:23

        It was the Gemzar.

    30. PAPeter Attia2:09:24

        Yeah.
14. 2:18:26 – 2:29:53

    Sarah’s reflections on her approach to life with chronic cancer and balancing her time

    1. PAPeter Attia2:18:27

       Sarah, y- you, you're very, um, realistic about the fact that your time on this earth is less than it should be, right? A, a, a 49-year-old otherwise healthy person who's done all the, you know, uh, done the right things for their health should have another 40 years on this planet, and at least statistically speaking, that's, that's not, doesn't seem likely. It suggests to me that you're very cognizant of how you spend your time. Uh, so should take a moment to thank you for spending a couple hours with me here. But how do you now think about the time that you allocate to your family, to your work in the diabetes community, and now to this third important pillar to you, which is cancer advocacy? H- how are you, how are you, how are you managing that, and, and how do you, how do you think about how to even balance that? Because I think time is the most important currency. I think everybody can appreciate that in a vague sense. It is the great equalizer. Um, but of course, most of us can't appreciate it the way you can because you have a real visceral appreciation for it that comes exactly with this type of an illness. Um, and so therefore, I think that your appreciation for the balancing act of what you described earlier, which is living your life to the fullest regardless of its duration, that's your legacy. That's what your kids are gonna remember about their mom, being the advocate for other patients so that in 10 years when another Sarah Hallberg gets this diagnosis, even if she doesn't have your education or your means, she can have ... an extension of life the way you do. I- it's, it's, it's a bit overwhelming for me to think about how I would do that. Because as I put myself in your shoes, my intuition is I'd want to retreat from everything outside of life, uh, everything outside of my family. Like I, I, I would imagine, uh, and, and it's hard to put yourself in another person's shoes without being there, but my intuition is I would say, "I don't care about anything outside of the walls of this house." And I would take a selfish approach in some ways, I think, and you've done this very selfless thing, which is continuing to sort of prioritize everything else as well. Um, how, how do you do that?

    2. SHSarah Hallberg2:21:05

       Well, a couple of things. You know, number one, believe it or not, originally it was, it was actually hard to be around my kids when I was so deep in grief because... And that sounds crazy, right? That sounds counterintuitive, but they reminded me of everything I was gonna lose, right? They were the, they were what I didn't wanna lose, and so it was challenging, and I ha- I knew I had to overcome that, you know? And that, that, that was, that was a big motivator for me to not be, you know, thinking about that, um, uh, and thinking in that way, and I, I'm happy to say I, I clearly have overcome that. But, um, my kids come first, you know. I'll drop anything and everything if they need me now. But I also think, again, and I go back to sort of what I alluded to before, they need to see me, um, not letting, not getting knocked out by the stressors and bad things in life, you know? I mean, bad things happen to good people, you know. I- like I said, there's been a pivot in every part of my career based on anger, and I certainly am angry about this, but what do you do with it? That's, that's what's gonna be the important question in life. You can take anger, you can take all these things, and you can get lost and buried in it, okay? Or you can try to turn it into, you know, something else. And I have to say, I haven't become as big a cancer advocate yet, and I'm working on it, but the reason for that is... And this was a question I had to ask myself a long time ago, which is, "Shouldn't you be a cancer advocate now?" Was, but I have a platform for diabetes, and damn it, that's important, too. All these people suffering from this is important. So I can't just say I'm gonna switch away from a platform that I have to one where I don't yet. It doesn't mean I'm ignoring it, but it's like it makes me wanna work more again for health equity because it spans both, right? It has to do with both diabetes, um, and cancer, you know. Um, a- and, and that is so important. So yeah, how I spend my time is really critical. And I wanna say it's not like I'm... I don't wanna paint the picture that, oh my gosh, I'm the superwoman. I have a terminal c- cancer, and yay, life is great. No. You know, when people ask how I'm doing, okay. If I say okay, you know I'm doing okay. There's never good or never great, okay? And that's just where I live right now. I'm definitely not sitting around and feeling sorry for myself, okay? Definitely not, not enjoying things in life. But great is hard to think about, you know. Great is hard to think about now. And, you know, the... Some people say, "Well, so cancer really helped me get a new perspective on life and what I care about." And, you know, I'm happy to say I don't know that I got that, okay? I mean, having cancer s- sucks, and I'm still mad about it, and, you know, sometimes I have to sit and have a pity party every once in a while because the fact of the matter is I loved my life pre-cancer, and I think I was living every minute of it. I think I cherished my children. I cherished vacations. I mean, you know, that, uh, I cherished travel and showing my children travel, and that's, you know, that's a bit of a wonderful thing, and it's also like a dagger, too. It's not like I've gotten some new life and new perspective that's so different from my old. Damn it, I liked my old life, and I liked the old me, and it's still a little hard to get used to who this person is now. She's still motivated. She still exercises, although not doing the things I used to. She loves her children with as much passion as one could have, but I'm, I'm fundamentally different. It's tough.

    3. PAPeter Attia2:25:51

       Sarah, you've, uh... You know, you've, you've said a lot of things that, uh, um, obviously resonate, um, um, and I think will, will resonate with a lot of people. So I, um, you know, I wanna, I wanna thank you from the bottom of my heart, [sniffs] and, uh, certainly wish you the best.

    4. SHSarah Hallberg2:26:25

       Thanks. I appreciate it.

    5. PAPeter Attia2:26:27

       It's, uh, it's been, it's been great knowing you through this journey as well. You are Uh, as many of your colleagues, uh, have, have, have undoubtedly told you, and we've certainly discussed it behind your back, uh, you are an inspiration. And nobody wants to hear that 'cause nobody [chuckles] wants to be the inspiration. You just want to be the normal person. But, uh, you are an inspiration.

    6. SHSarah Hallberg2:26:48

       Just want to be a normal person. Yeah.

    7. PAPeter Attia2:26:49

       Yeah. Well, thank you for setting aside time.

    8. SHSarah Hallberg2:26:54

       Thank you. Yeah, and I mean, I thank you so much for having me on. I mean, believe it or not, this is the first time I've told my story, you know, um, in any way, shape, or form. So I have been kind of preparing for this, um, and I, I'm glad I did it. And so thank you for giving me an opportunity to do that. And thank you.

    9. PAPeter Attia2:27:23

       Thank you for trusting us. Thank you for trusting me and the listeners. [upbeat music] Thank you for listening to this week's episode of The Drive. If you're interested in diving deeper into any topics we discuss, we've created a membership program that allows us to bring you more in-depth exclusive content without relying on paid ads. It's our goal to ensure members get back much more than the price of the subscription. Now, to that end, membership benefits include a bunch of things. One, totally kickass comprehensive podcast show notes that detail every topic, paper, person, thing we discuss on each episode. The word on the street is nobody's show notes rival these. Monthly AMA episodes or Ask Me Anything episodes, hearing these episodes completely. Access to our private podcast feed that allows you to hear everything without having to listen to spiels like this. The Qualies, which are a super short podcast that we release every Tuesday through Friday, highlighting the best questions, topics, and tactics discussed on previous episodes of The Drive. This is a great way to catch up on previous episodes without having to go back and necessarily listen to every one. Steep discounts on products that I believe in but for which I'm not getting paid to endorse, and a whole bunch of other benefits that we continue to trickle in as time goes on. If you want to learn more and access these member-only benefits, you can head over to peterattiamd.com/subscribe. You can find me on Twitter, Instagram, and Facebook, all with the ID PeterAttiaMD. You can also leave us a review on Apple Podcasts or whatever podcast player you listen on. This podcast is for general informational purposes only and does not constitute the practice of medicine, nursing, or other professional healthcare services, including the giving of medical advice. No doctor-patient relationship is formed. The use of this information and the materials linked to this podcast is at the user's own risk. The content on this podcast is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Users should not disregard or delay in obtaining medical advice from any medical condition they have, and they should seek the assistance of their healthcare professionals for any such conditions. Finally, I take conflicts of interest very seriously. For all of my disclosures and the companies I invest in or advise, please visit peterattiamd.com/about where I keep an up-to-date and active list of such companies. [upbeat music]

Episode duration: 2:29:53