The Peter Attia Drive - In remembrance of Sarah Hallberg, D.O., M.S. (Ep. #162 Rebroadcast)

Episode Date: April 4, 2022

View the Show Notes Page for This Episode Become a Member to Receive Exclusive Content Episode Description: Today’s episode of The Drive is a rebroadcast of the conversation with Sarah Hallberg��(released on May 17th, 2021). It's with great sadness that we report that Sarah recently lost her battle with lung cancer, and as such we've decided to republish her episode to honor her amazing work in challenging the status quo in the treatment of metabolic disease. Sarah Hallberg was the Medical Director at Virta Health and a physician who spent nearly two decades treating patients with obesity and type 2 diabetes. In the first half of this episode, Sarah discusses how she became a huge believer in the efficacy of carbohydrate restriction for the treatment of type 2 diabetes through her research and clinical experience. Sarah challenges the common beliefs about the role of dietary fat and carbohydrate on the plasma makeup of fatty acids and triglycerides. She also expresses the importance of understanding early predictors of metabolic illness—highlighting one particular fatty acid as the most important early predictor—before finishing with a discussion about how doctors might be able to personalize patients’ metabolic management in the future. In the second half of this episode, Sarah tells the personal story of her own lung cancer diagnosis. She talks about dealing with her grief, deciding to continue her work while prioritizing her family, and how she devised a plan to extend her survival as long as possible.  We discuss: How Sarah discovered the profound impact of carbohydrate restriction for reversing obesity and type 2 diabetes [2:00]; Prediabetes and metabolic syndrome: prevalence, early signs, and the importance of treating early [14:45]; Overview of fatty acids, how they are metabolized, and understanding what you see in a standard blood panel [28:00]; The relationship between diet composition and metabolic markers [34:00]; Why palmitoleic acid is such an important biomarker [47:00]; The best early indicators of metabolic disease [58:45]; Personalized management of metabolic illness [1:05:45]; Sarah’s cancer diagnosis and the beginning of her journey [1:14:00]; The emotional impact of a devastating diagnosis [1:26:00]; Sarah’s plan to extend survival [1:35:30]; Sarah’s aggressive treatment plan [1:46:15]; Life-threatening complications and the return of her cancer [1:57:45]; Sarah’s reflections on her approach to life with chronic cancer and balancing her time [2:09:45]; and More. Sign Up to Receive Peter’s Weekly Newsletter Connect With Peter on Twitter, Instagram, Facebook and YouTube

Welcome to a special episode of the drive. Today's episode is going to be a rebroadcast from an episode released in May of 2021, in memory of the guest Dr. Sarah Halbert. This podcast, Sarah and I, really talk about two completely different things. In the first half of the podcast, Sarah discusses how she became a believer in the efficacy of carbohydrate restriction and the treatment of type 2 diabetes through her clinical experience. She challenges the common beliefs about the role of dietary fat and carbohydrates on the plasma makeup of fatty acids and triglycerides, and also expresses importance in the understanding of the early predictors of metabolic illness.

But it's the second half of my conversation with Sarah that I really want to highlight. The second half of this episode is perhaps one of the most emotionally riveting discussions I've had on this podcast. It's one in which Sarah tells the personal story of her own lung cancer diagnosis and her journey through that. Sarah was diagnosed with lung cancer at the end of June of 2017, despite having never smoked and only being in her 40s. The time she was diagnosed, she already had stage 4 metastatic disease. disease, and I'm very sad to say that I just learned yesterday at the time of my recording this introduction that Sarah passed away from a very long battle with lung cancer. For those reasons I wanted to re-broadcast my conversation with Sarah as I believe it's something that, frankly, everyone would benefit from listening to even if you've heard it

once before. While it was admittedly a very difficult discussion to have with Sarah and while I can't even imagine how difficult it was for Sarah to have that discussion with me, I feel like it was an enormous privilege. And I think that those of us who knew Sarah will be forever grateful, and I think that many people listening who did not have the privilege of knowing Sarah, will still be indebted to her for what she shared in terms of her, her zest for life, and the manner in which she fought this disease and didn't really let it rob her of who she was. So without further delay, here's a special rebroadcast in memory of Dr. Sarah Halberg.

Here's a special re-broadcast in memory of Dr. Sarah Halberg. Welcome to the show. I'm super excited to be speaking with you today. This has the potential, of course, to be a 10-hour podcast, which it won't be, but I think that speaks to the depth of insight that you've got into so many topics that I actually want to talk about. Thank you. It's great to be here. Well, in thinking long and hard about how to navigate

all the threads I want to pull on, I figured we would just start with the nerdiest of all topics, which is something that I know you're so passionate about and yet 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? Well, 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 get more fat in your muscles, in your liver, and it's going to lead to increased insulin resistance, and thereby default going to lead to increased cardiovascular disease.

And we know that a therapeutic carbohydrate restricted diet brings down so many cardiovascular risk biomarkers that we're all used to hearing about. Okay, it decreases triglycerides. Okay, it actually can reverse type 2 diabetes in most cases and certainly significantly improved glycemic control in all. 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. And in future diabetes risk as well. But again, 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. So maybe taking even a greater step back from that Sarah, what is it that attracted you personally as a physician towards the management of type 2 diabetes because I mean that's how you and I got to know each other was through a company that you're a big part of called vertahelth, which I'm sure at some point today we will talk about. But what attracted you to this patient population and how is it that you stumbled upon the idea that there was 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 drugs? Well, I tell you, it's by accident.

If you had told me 20 years ago that I'd be playing this role in the healthcare system, I probably wouldn't have believed you. 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. I grew up as a product of the 80s, like so many people, where was the dogma, and there was no other way. And of course, entering into college and grad school, where I got both my bachelors and masters and 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, I'm bored certified in internal medicine, it was more the same. But again, it was so frustrating to me all along the way, really, to be continually giving this advice and then have people show up being worse. 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 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? 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. And as luck would have it at Indiana University Health, they knew about my background, knew about my past work at obesity care, and asked me to start a program, 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 was this going to look like. How are we going to tackle the untackleable, 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 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. Listen to some lectures by Dr. Steve Finney and Jeff Fulick, 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 cognitive dissidents overcoming that what I had been saying for well over a decade to so many people was really not found it 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 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 was astronomical. Hundreds of units of insulin. First of all, there's two questions.

I guess I want to ask you one, where are these patients primarily patients with type two 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. As you probably can imagine, when patients come into an obesity clinic, most all of them, if not all of them, have some form of metabolic disease, 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 a head off the potential resistance that was going to come. There was just no question of it. So I actually went about and spent an entire summer meeting with all the departments in

our local med center. And giving them a 15 minute slide presentation of when your patient comes back says that Dr. Holberg 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 didn't get any pushback. I actually pushed it even to the next level.

I was part of that time of the ambulatory quality committee at our institution, and I actually brought up a 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 Inchanged my life, right? And again, 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 because I was like, where is this? Where's this in the guidelines? How come I've never heard of this before? I mean, this is, I mean, I hate to be like over-dramatic, but it truly is quite miraculous for a disease that everyone thought was chronic and progressive to see people recover from it. It's 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 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 is much money. So I talked about that study presented it at the National Lippet Association quite a long time ago, talked about it actually in my TED talk, and then was speaking at the Obesity Medicine Association quite a long time ago and actually met Dr. Steve Finney, and that really changed the course of my life as well. So all this time you're sort of putting into practice what Steve and Jeff had been writing about for a long time and obviously Steve is someone I've been dying to have on the podcast and we were actually supposed to do it at one point in time and then scheduling got in the way. But 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 which was when I started implementing some of these treatments, I'm just a bow in a Chinashop. I just reached out to Steve right away. I might have been one of the first people to get a copy of the book that he and Jeff wrote in 2011, and I think I got a preprint of that book, which I still have, by the way, the Art and Science book, which I have. It might have more highlights and post-its in it than any book I am. Because I think like you, I was kind of going through the, this can't be.

There's something so counterintuitive to this that I need to read this over and over and over and over, we're going to make sure I get it. So it's funny 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 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, how was your experience being, how was that met? Well, it's interesting.

If I was speaking with someone who took care of obesity patients for obesity, they were totally, I get it. I'm doing the same thing to some varying degree, but when you moved out of that space to other sub-specialists, the first thing was, oh yeah, their diabetes will go away, but you're going to 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, you know, I don't know here in my practice, I had thousands of patients that would beg to differ with it. And I was like, I don't know. Here in my practice, I had thousands of patients that would beg to differ with that. And so those are the feedback that I got.

And one of the things was I knew that there had to be even more research done. I mean, we had wonderful pioneers in Steve and Jeff and Eric from Duke, Westman. But we needed even more. They needed to be larger trials. They needed to really specifically focus on patients with type 2 diabetes because I was convinced almost from the get-go that that is the target population here because that's where we see the biggest improvements. So this chance meeting with Steve at

obesity medicine association conference led to a dinner and led to funding of the large clinical trial that were 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 looking at nutritional ketosis as a means of reversing type 2 diabetes and pre-diabetes, which I'll just kind of stick in really quick here. Today actually happens to be the day that the pre-diabetes 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 at a conference. We haven't published the pre-diabetes results until today. So this was a paper that looks at the first two years of pre-diabetes utilizing a remote continuous support to help patients adhere to a diet aimed at nutritional ketosis. And Sarah, these are patients who defined as pre-diabetic by hemoglobin A1c. Correct. And that's being defined as 5.7 to 6.4. Is that the range? That's correct. Yes. being defined as 5.7 to 6.4, is that the range? That's correct. Yes. Okay. Tell people what that means. I think most people are aware of what a hemoglobin A1C is, but what does that translate to in an average glucose approximately? Yes, 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 do have to say here, though, that doesn't mean normal glucose is 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 can't be overstated again. But in this study, we're looking at people who had insulin resistance long enough that

their pancreas in 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 two diabetes could be made, but once again, where we see the impact of insulin resistance where we see the impact of insulin resistance affecting the body's ability to keep blood sugar normal, due to pancreas being overworked for far too long. 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 U.S. population has type two diabetes. Is that approximately correct? Or is it more than 10% now? Approximately, with also the caveat of much more concerning levels in different minority populations, which, of course, hopefully we'll get a chance to talk about later, is just a huge goal with improving health equity in this country. So if it's 10% in all comers, do you have a sense of what it is in Hispanic and African-American populations?

Yeah, it gets even higher. It's well into the teens and those in Pacific Islanders as well. So these are populations that, you know, we need to be paying attention, of course, to everyone who has type two diabetes. But we also need to be paying attention to who's at greater risk. So what percentage of the population do we believe is formally in the pre-diabetic 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 Jerry Schoelman, which is one of my favorite discussions ever on the topic of insulin resistance.

I mean, Jerry really laid out elegantly the long time course of this disease. And even if you have normal fasting glucose and fasting insulin, but that early sign of elevated post-prandial insulin is really that early sign of insulin resistance that will then lead to post-brandial 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 pre-diabetic quote-unquotes I mean this has been a process that's been going on for five to ten years What is our belief about how many or what percentage of Americans

just to make it American centric for a moment? What percentage of Americans are in that bucket? Well, I tell you, recent studies will show us that over 50% of Americans, adult Americans, have diabetes or pre-diabetes. And a study released a couple of years ago, and I mean, this should shock everyone to its core based on N-haines data, that 88 per cent of Americans are not inoptible metabolic

health. I mean, let me say that again. 88% of adult Americans are not inoptible metabolic health, and that is by looking at Enhanes data and taking a look at the criteria for metabolic syndrome. And so the 12% are those who didn't meet any of the criteria for metabolic syndrome. I mean, that's frightening. Yeah, so I was gonna ask you

if that's exactly what it meant. So just let's state for the listener what metabolic syndrome is. We've certainly discussed it in 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,

though they do not have elevated blood pressure. And they're not on medication. 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 1.30 over 80. In our practice, we advocate less than 120 over 80. They have normal fasting glucose.

And that's defined as less than 100. 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. 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 trunkal 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 still the latest. Well, yeah, and I will also point out one really important thing here when it comes to waist circumference 2. 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 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 insulin resistance. They tend to have normal triglycerides and HDL. tend to have normal triglycerides and HDL. And so again, we can't be treating everybody the same, but we often do.

I'm glad you pointed that out. I still remember, it was about 10 years ago when I learned that lesson, which was taking care of an African-American patient who had about the most uncontrolled diabetes I'd ever seen. He may globe an A1C of 14%. This is a person who's basically gonna have their limbs amputated in the next hour.

Trigless rides of 89. Just, yeah, just totally normal. You look at their lipid panel, you wouldn't think anything is wrong. Right, and so that's the thing is they can get missed. And so knowing this and educating people on things like this again goes back to our working on health equities. And it's so important and so often not something people take into account. And just going back to pre-diabetes, the most

frustrating thing, I shouldn't say that it's one of the most frustrating things. There are many things about our healthcare system I could enter into the most frustrating. But one of them is patients coming in to see me whose lab showed prediabetes. And I said, oh, you have prediabetes. Oh, no, no, no, my physician said I was fine. The fact that we don't appreciate that by the time you get to pre-diabetes, there's some really serious things going on here. Their vision is being impacted. Their nerves are being impacted. You know, these are things we can't just say, oh, they haven't gotten bad enough to bother with because they're not at the criteria for type

two diabetes yet. I mean, we have to pay attention. And so if that's one thing, if there's any physicians listening, which I know that there are, don't ignore any elevation in blood sugar. That means there's been a problem for a long time already. And patients should be also hypervigital in about this. I mean, I've seen patients in that prediabetic camp, and this is using an example of a male patient, when their insulin sensitivity is restored and their blood goo close, comes down

by an average of 10 milligrams per desolate, they'll say, wow, I have better erections, all of a sudden. And that speaks to even the microvascular damage that's being done long before you get to diabetes. You know, actually was exchanging emails with a really good ophthalmologist recently and kind of trying to ask how far are we away from being able to use retinal imaging as a screening tool for early, early, early, microvascular disease because I think the hemoglobin A1C is just far too crude a metric for this. And I actually have seen some interesting literature and I'm

sure you've seen even more of it that suggests that this is, you know, if you look at the microvascular in the eye, it might be one of the earliest warning signs of when things go awry. And so in an ideal world, I would love it if we had tech that basically allowed for quick and easy evaluation of that. So that to your point, it doesn't really matter if your tricks are up or down and your waist is big or not. Like let's look at the actual place where the damage is taking place and make the

assessment on an individualized basis, as opposed to using these sort of population-based metrics, which move in the right direction, but for anyone individual, it can be quite misleading. Yeah, and then I love the eye discussion because one of the other, I think, really important questions is once we do get to damage, can we make it better? Can we make it better without and skip some of the horrors of having diabetic eye disease for millions of patients? I mean, that is a really burning question for me and one that I think we need to really explore. Yeah, indeed. So with that background,

let's kind of dive into some of this nerdy, nerdy fatty acid stuff. And I got to 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, 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, mono unsaturated fats, and poly unsaturated fats. The saturated fats have no double bonds, so that means every carbon is fully saturated with hydrogen. The mono unsaturated have one and only one unsaturation, 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, which is the C16 saturated fat. So can you talk a little bit about how abundant that is and what our body's options are for? What it's called, let's start with the nomenclature. What does pure C16 look like? That's pulmitalitic acid.

So it's really interesting what happens. And do you mind if I jump on and share screen here so we can talk a little bit more about it? Yeah, that would make it easier for everybody, I'm sure. I want to start by talking about saturated fatty acids in general. 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, that is correlated with insulin resistance and adiposity, likely reflecting accelerated hepatic denoval lipogenesis or also it can be what is actually returned to the liver. So really too. We certainly know that hepatic denoval lipogenesis is a big part of the problem when it comes to elevated triglycerides, but we can also make these with some, what is delivered exactly back to the liver.

And so when we see saturated fatty acids as a makeup of triglycerides or maybe even the phospholipids there, 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, 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. Sarah, can I explain a technical point on this slide that you and I will take for granted, but I want to make sure that a listener understands. So 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 desoliter. LDL cholesterol equals 140 milligrams per desoliter. Triglisterides equal 150 milligrams per desoliter. HDL cholesterol is 35 milligrams per desoliter. And VLDL cholesterol, if I remembered the numbers, I just spit out, would be 25 milligrams per desoliter. 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 LIPA proteins. 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 when it comes to measuring the triglyceride, we want to eliminate what's in the chylamicron.

We want to measuring the triglyceride, we want to eliminate what's in the chylamychron. 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 let me restate that because 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 desolate, that's basically saying, look, 90% of that 150 milligrams per desolate is within your VLDL cholesterol. Some of that is an intermediate density lipoprotein, but that's virtually nonexistent. There's a trace of that in the LDL cholesterol and even a smaller trace in the HDL, but the lion's share is in the VL-DL cholesterol.

And as you're gonna 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 going to become very important in this discussion. Absolutely. Yeah, and that's really important. Thank you for the precursor explanation,

because this is technical stuff, and that is really important for people to understand. Then the next question really becomes, okay, so if we have a high saturated fatty acid content within the VLDL, okay, again, it's being in the triglycerides, the phospholipid membrane, wherever we find it, where did the saturated fatty acids come from? 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 by Dr. Brittany Volk 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 were 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 346 grams, which was C6 feeding phase.

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 guideline on saturated fat. I mean, so far above what anyone would consider at goal. And then we get down to the C6 and we're much less 32 grams. Again, what happens to the fatty acids as people are run through these six phases? 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.

Correct. They did not. And so what happened over these six phases? So here we have saturated fatty acid levels marked. Okay, so here's the baseline at that run-in. And we see when we have the very high saturated fat level, very low carbohydrate, 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, 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 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, it can make more sense. I mean, it's actually statistically insignificant in terms of C16, right, which is the dominant saturated fatty acid. So, so, so, palmitic acid, it trended towards an increase as saturated fat, dietary saturated

fat went down and carbohydrate went up, but it didn't reach significance. And the only one that actually did significantly increase was C14, right? Yeah, actually C161 as well. And that one is we're going to spend hopefully a little bit of time on. Yeah, yeah, no, but as a saturated fat, it was really just. Oh, as a saturated fat, yes. Yes, yeah. 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 very high saturated fat

diet. Essentially, and this is important, it stays the same. If anything, there's a trend 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 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? 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, but you also store it within the cholesterol ester. And it's 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. 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 16-1. That's plummet-alaiic 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. So moving on,

one other trial that shows this and then we'll bring up the table that I had erroneously brought up for the first study. But 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 Volick's group from 2008. And what I like here is you can see very readily with these pie charts exactly what the content

of the two diets were. So again, we really have it flipped. 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 3 times as high in the low carb diet at 36. These are both really low calorie studies. Was this an adlib feeding study or were these deliberately calorie restricted? How has this study done?

Yeah, these were both that wanted the calorie intake of the two studies to be the same. So as you can see, there were about 1,500 calories a piece. And were they deliberately calorie restricted? Yes. So what we can see here is that what we have when we take a look at these two arms is taking all look on the right to the change in serum saturated fatty acids. We can see in the carburestricted diet, significant decrease versus the low fat diet. So again, in the much higher saturated fatty acid arm, we see a significant decrease down,

whereas we do see a drop in the low saturated fatty acid intake group, but not merely as much as we see with the carbohydrate-restricted group. Once again, arguing against, you are what you eat. And I want to now get in a little bit more to this. What I think is actually even more important, which is the change in the pulmitaleic acid. Yeah, so pulmitic acid is 16-0. Pulmitaleic acid is 16-1. They look almost the same except that pulmitaleic,

the 16-1 has that double double bond at the N7 position. And you're going to explain in a moment which enzyme does that and why that matters, right? Right, absolutely. You know, what is it about this? It's not a saturated fatty acid. So why do we care so much what happens to 161? But it's pretty evident here what happens first of all, and then we'll talk about why. What happens is that with 161 in the high saturated fatty acid group, it drops significantly. We're in the low fat group, again low saturated fatty acid group,

it actually goes up, and this is a statistically significant difference, okay? Much more significant even as we look than the change in the serum fatty acids. So now I'm going to pull up a graph of these results to look at it a little better and then I want to get into the actual science of it. This is the very low carbohydrate arm on the left and it is the low fat arm on the right. And so what we see here, and we look at total saturated fatty acids, is that it has dropped 5% between the low carbohydrate group and the low fat group, total saturated fatty acids. And what we see here with the 161 and much more significant statistically is that we see between a low carbohydrate diet and a low fat diet that we have a more significant decrease

in the 161 with the low carbohydrate higher fat diet. So there's a couple things going on here for people that are going to be overwhelmed by this table. And I apologize if you're just listening to this without watching it on video, I'll do my best to explain what's going on here. So the first thing to notice here is both of these groups of patients started out with quite elevated triglycerides. So in the first group, in the group that was randomized

to the very low carbohydrate diet, their average triglyceride at the start of this study was 211 milligrams per desolate. That's sky high. At the end of 12 weeks, it was down to about 104 milligrams per desolate. It fell by about 50%. Conversely, the group that started out in the low fat arm also very high triglycerides to start 187 milligrams per deciliter.

By the end of 12 weeks, they saw about a 20% reduction to about 150 milligrams per deciliter. Now, this is where these tables get a little bit confusing because the table is showing both the relative and absolute reduction of the relative amount of saturated fat reduction on a relative basis, both groups saw slight reduction. But it was statistically more significant in one group than the other. The low carb group was a 12% reduction versus 5% in the low fat group. And on an absolute basis, that difference was even greater because the low carb group

had such a significant reduction in total triglyceride as well. And that's the dominant source of where you're going to see these fatty acids. And of course, the reverse is true when it comes to 161. So let's now ask the question, Sarah, what is it about palmitaleic acid that you think is such an important biomarker? Because we wouldn't be having this discussion if you didn't think we should be paying attention to this. I think it's a really important biomarker.

And if you would allow me, let me point out one other thing here regarding the triglycerides because clearly the low carbohydrate arm decreased more in the triglycerides. 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. But I do want to remind everyone that this was a calorie restricted, this was around 1500 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. I think pulmitaleic acid, or again, that's that 16-1, is really not appreciated as the health predictor that it really is.

Okay, so let's go through. I'm going to just jump ahead a little bit here. So, pomodalic or we like to call it POA is a product of something called sterile coa desaturase. And sterile coa desaturase is going to determine what is going to happen with some of the fatty acids in our system, specifically what's going to happen to POA. Now what we know ahead is that sterile co-a desaturase is actually an independent marker of triglycerideinia and abdominal adiposity. So in other words 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.

So if we have a high levels of sterile co-aid desaturase activity, right there we got to 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 the earlier part of our conversation, where we say so many times these things are missed, people can still have normal blood sugars, it's going to 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. So plasma triglycerides, and let's take a look at, again, POA in those plasma triglycerides in the way of looking at it in quartiles. So again, low versus high. What we can see is the POA, the byproduct of sterile co-Aaturase is much higher, the higher the triglycerides are. Very important. So if your triglycerides are really high, again, what's happening low-ary likely is that your POA is elevated as well, brought about by increased activity of sterile co-A desaturates. And this shouldn't be surprising, right? Because if you look at the very unfriendly diagrams of fatty acid metabolism, one of the first steps we see in the conversion or elongation of fatty acids is the conversion

of C160, palmitic acid, into C161, palmitoliac acid, and 7 through an enzyme that has two names, I guess depending on the naming of nomenclature, right? So delta 9 desaturate, desaturate the number nine carbon from the delta end, also known as sterile co-a desaturase, which I think is the more popular name is SCD1, right? Right. And if you go down that pathway, what you're basically doing is bundling

and packaging fat to leave the liver, right? Yes. And here is one of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of the bad idea of One would have to wonder, is that a protection mechanism? Why do we want to do that? 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. 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? All right, well, let's go through it really quick and then get to answering that question, because I think it's really important and really shed light on why we need to be paying more attention to the all-important POA, and of course the precursors and enzymes that act in its creation. So let's go through, if you will,

this cartoon that I know looks really busy initially, but let me just kind of run through it, starting here in the intestine. And remember, we'll start off by saying, our focus in healthcare 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 are slowly absorbed carbohydrates, are starches. Okay? And what happens when they come in as glucose, that feeds in again

through glute 2 into the pancreas, pushing out more insulin, insulin then feeds into the liver. And what we get here is going through a big, big part of this is SREBP1. 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 SCD1 or sterile coa desaturase, increasing. Very important. And it comes about through other means as well, fructose coming in through glute 5 or glucose coming directly into the liver through glute 2. They're all feeding into this by slightly different mechanisms to increase this SCD1.

Now we're gonna look more at the process in a different way. So we have increased hepatic, first of all, saturated fat. Okay, here's our 16-0, the saturated fat. Increase hepatic levels of this. What gets turned on as from the past cartoon, we get that increasing that leads to this increase in POA. Coming down here, what's the end gain here? Increased VLDL. Same thing over here, looking at it different.

We see, again, SCD1, if it's blocked, we won't see that. 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 P O A. 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. 16-0 saturated fat is elevated and it turns on this cascade leading to increase in the LDL. Yeah, again, I think for folks that are watching this, it's going to make a bit more sense.

And if you're not, I just want to make sure we're bringing you along for the ride. So in the liver, when you are taking C16 or C18, but let's just keep the discussion simple and start with a saturated C16, the first committed step is going through SCD1 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 in 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 and hand with non-alcoholic fatty liver disease, which is truly an epidemic at the moment. 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. 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, which is not to say that the inflammatory environment that comes with it doesn't pour more gasoline on that fire. But you know, it is my belief that everything we're talking about here is the body's aim to protect itself from an abundance of nutrition. And so that's how I read this is the body is doing, and specifically the liver, which

is arguably the most important organ in this situation, and the liver is 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 tolerance for carbohydrate consumption. 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. Would you agree with my teleologic view of that? I 100% would agree with it. And again, I think that we are going to have more and more details on this coming out very soon

in many research projects that are currently ongoing. But what it really comes down to is we want to know what an individual's carbohydrate tolerance is. OK? 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 going to happen with the patient right in front of you. We really want to know what the individualized reaction is going to be. 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 want to 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, they're individual tolerance. That POA level is going to be a great biomarker. It's going to go up as again a protective mechanism in the liver. Our livers are really, I mean, 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.

And so again, I want to also go back on one other thing that you said. And the other thing that you said is, so this comes 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, itself that causes obesity. So we have to really take that into account when we're in the office with someone who's struggling with obesity. And I know Peter, you take this really to heart, approaching and treating these patients without bias as I do. But it's so important for other providers to be looking themselves in the mirror and asking themselves, what are the biases I hold against patients who come to me struggling

with their weight? And what do I really know about the science? And what it really, one must conclude is that this is not their fault. 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. So Sarah, I want to keep digging into this idea because it's so interesting

to me of having a leading indicator for, you know, this early, early, early warning sign. We talked about it at the outset of this discussion, which is 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 that literally is happening 10, 15, maybe 20 years after there were early, early molecular warning signs. And if measuring palmitolic acid is one of them, that's exactly the kind of stuff that

I find interesting because in our practice, we use CGM a lot. So continuous glucose monitoring, 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 palmitolayic acid and triglyceride is so tight

that would we miss, for example, African-American patients? Do we know if they're failing to synthesize C161 in the way a white patient is. 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, and actually worse middle or upper middle class white people. So there are a lot of questions with this in specific populations.

There have been a couple of studies recently coming out looking specifically at what we're talking about, POA, and it's marker for future problems and predictor of future diabetes and other issues. One was a study recently published future problems and predictor future diabetes and other issues. 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, where they looked at POA levels at 50 to correlate them with C-reactive protein levels at age 70. And what we see is what we would expect based on 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. What we really want to know ahead of time, and I know this is very meaningful to you and your practice, is I want the person who's healthy, so I can get to tell them how to stay healthy.

We talk a lot about trying to work on people who are already, 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. Again, I hope there's an ongoing effort here because I think this is the future of medicine, right? I mean, I think the future of medicine has to be coming up with tools that allow us

to take broad sweeping population-based insights and very quickly 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? Again, you and I have a very similar set of experiences, which is patients with hyperinsulinemia and elevated glucose generally respond well to carbohydrate

restriction. My practice also focuses so much on the role of glucose disposal and non-insulin dependent glucose disposal through exercise. And I know that that's probably not a surprise to many people is sort of correcting the sleep exercise nutrition, trifecta. And I know that that's probably not a surprise to many people is sort of correcting the sleep exercise nutrition, trifecta, and then adding to that the the role of cortisol and all of this. So 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 your risk of heart disease, cancer, Alzheimer's disease, all go down. And so it's worth this enormous effort to continue pushing on these questions. On that note too, and when we talk about individualization and risk prediction

before we're seeing our classic biomarker issues come up, has to do, I'll circle it back to carbohydrate restriction because we know very low levels of carbohydrate restriction can reverse the disease process, bring about normal glycemia in patients and be able to get them off of medications. But 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 were like, hey buddy, you go over you know 175, that's where trouble comes in. Rather than you need to stay very low indefinitely because we've caught you on the spectrum of the disease 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. I want to ask you another question on this, Sarah. And again, I don't know if it applies to patients that you've treated with diabetes or those in the pre-diabetes category, but 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 maybe spent years on a carbohydrate-restricted protocol. And everything gets better. So 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. How often do you see that and what do you think is the best explanation for that? See it all the time and the best explanation for it is what is their insulin reserve. So majority of people can go ahead starting out even at long-standing diabetes, reverse their disease, get normal glycemia, get off of all their medications, and then slowly reintroduce carbohydrates as long as they have functioning beta cells. The problem is the longer you've had diabetes clearly is a risk factor for this can, we see evidence of that in the bariatric surgery literature as well. I mean, there's been so many studies looking at beta cells.

And the fascinating thing is who is getting back some of their beta cell function? In other words, maybe their beta cells were only dormant and were able to 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, a lot of the changes 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, logic would tell us that some sort of beta-self function has returned. It took a long time. Reset the system, help them heal. 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. Because the answer on the personalized level is, how many am I in a dormant? How many am I in a dead?

What's it going to take for me to wake these up? If it's impossible, I'd like to know that because that sets expectations ahead of time, right? You can get a lot better, but there's always going to be a little insulin in your life. It doesn't mean if they are someone who doesn't have any insulin 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,

why is this happening that some people can start to eat carbohydrates, not anywhere near to where they were, but they're able to put some back into their diets versus people who can't is beta cell function. Something in there that you said is very important that I don't think 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 ladder over the former all day, every day, non-negotiable. 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. And let's put the economics aside. The economics are enormous, but ignore that for a moment, just in terms of health outcomes, the negative effects of

hyperinsulinemia. I just want to say with that, you know, if we really think about the way we manage diabetes, 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 of 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 going to give this medication, this insulin that you're going to inject to you. And I'm going to do that because your blood sugars are so high that they could acutely kill you, 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 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. Yeah, I agree. So I want to talk about something that has 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 good discussion could basically continue down the path that we could talk more about diabetes. We could end this discussion here and people would say, wow, that's a really insightful, thoughtful person. But there's a whole other side to your experience with health care, a Sarah that started gosh, four, you're almost four years ago.

I'll tell the beginning of this story just from my end. So you and I obviously met each other through Verta, your early part of the creation of this company, which is basically scaling up a way to remotely treat patients with type two diabetes. This is a company that Steve Finney is also a co-founder of along with Jeff Olic, I believe. I have a minimal involvement in that company. I'm a small investor and at one point was an advisor, but it was during one of these advisory meetings that you and I happen to be sitting next to each other. Now we've 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, you-shaped table in the room, and it was a two-day ordeal, and you were sitting to my left, and that gave us more time than most times to be chatting about this, that, and the other thing, and you looked in perfect health, as always, and at the end of the second day I said goodbye and see you next time in blah, blah, blah, blah. And then about a month later I heard from a mutual friend that you had been diagnosed with lung cancer, and I just about fell off my chair. So can you tell people what happened that summer, the summer of 2017? Yeah, so I'll just start by saying,

I've been someone who's taken care of themselves to the max all my life. Eatin' well, I've kept my weight in a normal weight, even nine months pregnant, I would have still been considered normal weight. Exercise like crazy, competed in half-marathons, triophilons, elliptic distance. I did everything right. Never smoked, never drank to excess.

And 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 due to my wonderfully full house of three kids and took a business call in the basement because that's always my escape place where it can be a little less noisy and all of a sudden I couldn't talk and I couldn't figure out what was going on. I knew something wasn't right, but I couldn't talk. And I couldn't figure out what was going on. I knew something wasn't right, but I couldn't speak. And all I know is that I hung up the phone at some point,

because I was embarrassed. I was remembering thinking he's going to think I'm drunk. 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,

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 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 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 as they thought it was a stroke, and so my poor husband was all the sudden tasked with, are you going to give her clot-busting medication or not? Because we think she's having a stroke, but low-in behold, the imaging showed a really large tumor in my brain.

Then they imaged the rest of me, and it turns out I had multiple tumors in my chest. And so they presumed correctly at that point that this was lung cancer, but I also needed emergency brain surgery. I remember most of this by people telling me about it. So anyway, the next day, I had a virgin brain surgery and then being a physician and lung cancer,

I was like, that can't possibly be. I have never smoked. How do I have lung cancer? I am the healthiest person I know. I remember being in the hospital, because of course you're on drugs and everything else 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? Because somehow that was just one example of how that's impossible. Talk about the stages of grief and denial, right? And being a physician and knowing what lung cancer meant, the next thing that came out of my mouth is I want to move to Oregon. Because I was like, I know what this means for me, and I know what this means for my family,

and I don't want to play any part in this. I don't want them suffering. Can you tell folks what you mean by that? Not everybody might understand the implication of what you're saying. I wanted to go to Oregon because they had physician-assisted suicide. Because I knew I have treated so many patients with lung cancer. I knew the horrible end. I knew what this meant. The suffering. Especially when it spread. Yeah, and it had spread everywhere. I mean, I had stage four lung cancer. The day before

I had been fine, a hundred percent fine, that morning I had exercised vigorously. And suddenly, in the hospital, recovering from a brain surgery being told that I have a rapidly fatal disease. And all you can think of in that moment of panic is your family. And so, my only thought was, I don't want them to watch me go. I want them to remember mom. go. I want them to remember mom. And so I mean, they began my so far almost four-year journey of a new me, you know, cancer changes you know, I mourn that person. Because I really, I like her. I mean, one of the things that I think is very shocking for people to understand is that it's probably between 12 to 14% of people who get lung cancer are not smokers. 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. And I believe that's true for male and female still. Yes, I mean by far.

Yeah, to think that such a high percentage, 12 to 14% could be non-smokers tells us this severity of this. 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 median survival, meaning if you took 100 people 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? Well, it depends on what kind of lung cancer that you have, correct? Well, it depends on what kind of lung cancer that you have and sometimes even eight months or less. Those were the stats that I knew when I was first diagnosed and 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 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. So it goes against everything.

Do we have any insight into why? No, and it's one of the things that's not being investigated as much. When you look at, okay, what studies have been out there, oh, we get the typical, you know, it's radon, it's 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.

So, the fact of who it's impacting and the fact that the demographics of the people that it's impacting are the healthy people. Unlike what we associate with 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 cancer rises. That's not this. It's young women and again, who have presumably done everything right.

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. But otherwise, it's not getting the attention it deserves. And these women really wind up 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 alch positive cancer.

I have the EGFR, specifically something called EGFR X-on-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. I hadn't been seen as many people with active cancer as I did when I was in primary care. And so I was quite frankly behind on some of the newer treatments and newer diagnoses, if you will, and we're talking the genomics of cancer, but for EGFR cancer, there was something called a targeted therapy. This class of medications is called tyrosine kinase inhibitors and 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, they can even in many cases have all of the cancer go away. It doesn't mean they're cured though, because it always comes back. And so, after initially, again, going through all these, I mean, I'll tell you the denial of grief stage. I want to actually ask you exactly about that, Sarah. I want to 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. 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. What do you remember of those days? Overwhelming grief to the point of not being able to think. You know, of course, I come and approach everything in life as a mother. 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. How old were your children at the time, Sarah? They were 7, 12, and 14. They were 7, 12 and 14, and they needed me. They still need me. And so, the grief is overwhelming about what I quickly realized is, I'm going to break my children's heart, and there's not a thing I can do about it. And to have that realization, because it comes quick, and have to sit with that,

is a grief I can't even explain. And so initially I just was, I couldn't handle the grief. 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 family was, see, I can't be sick. I just got out of this brain surgery.

I'm still on medication. I walk seven miles today. I'm healthy. I don't know what you people are talking about. What did your kids know at this time? Did your husband already spoken with them? 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. That was never an option for us. So, they knew I was having surgery, that there was a tumor in my brain, This is not good. And that's a lot for a kid to unpack. Right? Especially a kid, you know, again, 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, everyone kid goes through it, the phase of, what if something happens to you, mommy? What if something happens to you, daddy, right? All kids go through that. And the one thing we used to kind of laugh together, my husband and I about that,

say, oh, honey, your mommy and daddy are the healthiest people. We are so healthy, you don't need to worry about that. And I remember that, you know, it's one of the first things that you think of when you're put in this situation is, oh my god. 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 diagnosis of advanced cancer. And we, it was a 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, I mean, my husband and I, is that we were never going to lie to them. We were always going to tell them the truth, because I thought that the worst thing for a kid is to constantly be wondering if there's going to be

a huge shoe that drops. And so we told them, we tried to open up the lines of communication, they mostly didn't want to talk about it, but we told them that we were making that promise to them, and we have never, never gone back on that problem, and promise never will. 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 going to hear about it. And over time, in grief, And as soon as we really know the facts, they're going to hear about it. And over time, in grief, you learn to accept many things. My husband and I, our dream, had been to retire to a farm and make gourmet butter. Like, that's what we were going to do. That was going to be the second career, right?

And you learn to make peace with that, not the case anymore. You know, we always used to joke that the way we wanted to die was 95 years old on the way home from a ski trip. In a fiery car accident where our kids would not have to deal with the bodies, but we wanted to make sure it was on the way home. The cremation, the two for one. A two for. It was going to be on the way home, because we were going to be having fun

up until that point. So that's acceptance. You know, you're not going to retire. You're not going to have all these things. But you can't accept that you're not going to be a mom impossible. Now, at some point, I'm guessing kind of the problem solver in you started saying, like, hey, I'm going to learn as much as can be known about this.

And we're going to talk about this in the context of the asymmetry that exists. I just had a discussion about this with we have a weekly meeting in our practice with all the providers. And you know, we just had this weird situation recently where, you know, basically a patient of ours who has another physician 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 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 going to have a surgery that they

totally didn't need. That's a very big surgery with lots of risks. And we realize that asymmetry of knowledge in medicine is so overwhelming that it is, it's not even just about money or education outside of medicine. A smart person still has a hard time digesting medical literature. And I feel like I said we're going to talk about this, but you know, you very quickly must have figured out, hey, I have this EGFR 19 deletion. So we no longer talk about this as you have lung cancer,

or you have ad no, or you have non-small cell. We're really going to 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 going to, I don't know if this is the right word, but I'm going to partition my grief and my problem solving brains. And I'll do both of them, but I'll move back and forth. It happened pretty quick, which is, okay, this is terminal, right? You have to come to grasp at that, but terminal when. And what can I do to control the when?

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 going to 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 going to take you to being the 95-year-old skier? Yeah, I mean, I think just reading and understanding, although the advances that this was going to 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. You're going to be 50 soon? Yeah, I'm going to be 50 in the not too distant future. So, you know, that was like my first one was just like, okay, let's... But right from the beginning, I'll tell you, the when was 11 years. Okay, and that has not left. I don't need to be 95. I can accept all those things that I'm going to 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. So immediately my goal was I can't settle for less than 11 years. I have to make it to 11 years. And so in became that like by war cry, 11 years, 11 years, I have to make it 11 years. And that started me on a path of, oh my gosh, so much. So the first thing I thought in reading all the, I mean, read everything is, I got to 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 of 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 advanced ones at the long and is like 24 to 30 months, okay? So that's not enough time. That doesn't get me to 11. So I was like, okay, you know, this is increasing the risk for mutation, which is how these develop resistance to the tyrosine kinase inhibitors. And remind me, Sarah, you, because I remember you emailing me probably by August and starting to explain some of the details, your biggest tumor was like five centimeters. That's a monster tumor. How many tumors did you have? It was six centimeters or you had six tumors. It was six centimeters,

which is amazing in the sense that I never had pain from it. I never had a cough. Probably because you were so healthy. I think so because talk about being caught out of the blue. You know, there just wasn't this premonition of something is a rye and I'm just not addressing it. So the standard of care was just that we typically don't operate on patients with metastatic tumors. It's it doesn't the only reason they operate it on your brain was it was an acute way to save your life. I think it's hard for patients listening to this to understand that, but 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 going to be dead probably within days if they didn't operate on your brain. But all this time, afterwards, you still have 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. Right. 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 slatters on throughout both lungs. And they were gone in a matter of weeks. That's staggering, isn't it? I mean, it is. It's remarkable. But, you know, again, the primary tumor was huge. So, I had, unfortunately, the large tumor in my brain was not the only one. I had two other ones

that they radiated. They didn't need to be surgically removed. They were small. They could be radiated. And then I said about trying to find someone who would take out this primary tumor. Can I ask you about the stereotactic radiation, Sarah? That's, I mean, we glossed over that, but that's not a benign process either. Did you suffer nausea from that? How difficult was your stereotactic treatment? Did you take it all and stride? I did great with the treatment to the brain. I didn't have any issues. I did have issues at the beginning, but they were more to the TKI.

One of the things with every specialist that I saw, they couldn't believe it or they told me, if I saw them earlier, it wasn't going to happen. At least you'll keep your hair, all my hair fell out. It wasn't going to happen, you know, at least you'll keep your hair, all my hair fell out. Like it wasn't supposed to happen. Hair is not supposed to fall out with TKI, it's all my hair fell out. Anyway, so the brain radiation went fine. And then I met a surgeon who was going to take out the primary tumor from the reasons that I was saying. We just, anything to decrease the risk of developing a mutation that keeps me from being sensitive to the TKIs. And so I went in 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 medias dynum. But there was no disease on the PET scan in the medias dynum. 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. And just so folks know what we're saying 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 medius dynum. And so you had this monster tumor that was going to 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 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? And that happened. And that was, it was terrible. I kept apparently, under the influence, 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 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 that was all that I kept saying. So, you know, I had to come home and learn to accept that. And now was bald. And I definitely fell into a deep depression but at the same time 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 which sounds crazy. But it's just part of this whole process and And then, but after the surgery failure, that was terrible. 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, I had been selected to be an Aspen Health Innovator Fellow, which was, I mean been selected to be an Aspen Health Innovator Fellow, which was, I mean, this is among the highest honors for your work. The Aspen Institute is a place that brings together thinkers in all kinds of disciplines and to be chosen to represent people who are innovating in the health care space

was 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, signed me up. But as that first session inched closer, it was in November. 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 got on the airplane. Because I was ready to run back.

Because it was like, I'm gonna leave my kids for almost a week. I've 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, I've cried on a lot of planes since this diagnosis.

Deciding, I just chose to live. This was a moment. I made my choice. Now I got to stick with it. And that's how I've tried to live my life since then. Because 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 lottery. So my god, you can win, you know, bajillion dollars. And so my husband and I were at the dinner table joking around about it, right? I mean, we don't play the lottery, but we were joking around, baby, 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 like, I was like, oh my God. You know, at the time I just... I was so taken aback by that.

Certainly that weighed heavily on my decision to get on that plane and to continue doing what I'm doing. 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, you know, one of the lucky ones. And I didn't realize the stark differences until I became a patient. I want to talk about that in some detail, Sarah, but I want to also understand how it is that we're still talking today, frankly. In other words, how have you managed to stay in an

equilibrium with this disease? I've always, I mean, let me share with you a couple of things that I've always struggled with when thinking about cancer. I'm not fond of the language that we sometimes use around cancer and that we beat cancer and that we can't give up and things like that, because it almost suggests that the patients who don't survive cancer have somehow given up. And I just don't find that in my experience, having taken care of many patients with cancer to be true, I think, you know, it doesn't make sense to me. And I think the way that you said it and described it earlier makes the most sense, which is basically

finding a way to co-exist with your cancer for as long as possible. You've exceeded all odds. I want to kind of understand that journey a little bit more. It's one thing to go through the tyrosine kinase inhibitor have this immediate response that's remarkable, but then get this setback three months later, where your primary is not only still there, but you actually realize now there's there's media-stinal involvement, which basically means there's no question you have cancer cells elsewhere in your body. 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 like. How have you stayed in this state of equilibrium, so to speak? So I haven't, okay. On many occasions, I haven't. So after the surgery, the next thing that happened is they found another brain tumor. There's argument as to whether it was there from the get go or whether it was something new, but either way

they decided it would be considered that the first line TKI that they had put me on had failed me. that they had put me on had failed me. And so I got switched to, I got more radiation to the brain and I was switched to the newest TKI. Happened to be called Awesome Mertonib or Chagristo. I was put on that in November, right before I went off for my first Aspen Leadership Conference and I had decided that I do not accept being a sitting duck because what the cancer world then 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 what's coming back soon. And 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 refused 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, 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'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 is worth a shot. February 2019, okay, because it took a long time to get to this point, right, of searching,

trying to find something. I started chemo, 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, because I had a very specific mutation besides the EGFR-1, 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 the chemo, I went on the anti-astrogen therapy. So I was put into early menopause with a number of regular medications, lupron, full of

strength, and then I was started on a medication called Pabla Cycleib, 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 Tigrisso or Asimurtonib. 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, single agent, very low-dose. So the first one was cisplatin. And everyone says, oh, cisplatin, you're going to do terrible on this. I mean, this is harsh. And you know, everyone says, oh, cis Platon, you know, you're going to do terrible

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

But anyway, some really wacky stuff that you do, but you just, you manage, you figure it out, right? You improvise, lots of improvising. And then I got switched to another after eight weeks, got switched to gem cytobene, or gemzar. Which again, these are so crazy, you just don't think of this because that's a drug that's typically used in pancreatic cancer, right? Well, yeah, and it can be used in lung cancer, too.

I mean, it just depends on the mutation. I think that's the point, right? Right. Yeah. Believe it or not, there's no standard chemo for lung cancer. Can you believe that? There's not a standard, like standard of care regimen. So the thing is, I wasn't doing any outlandish things here.

Okay. These are all treatments for lung cancer. Like you said, Gems are, 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, none of these things are, 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 something, you know, that's never ever been done before, you know, so to speak things. And at this point, which is now the fall of 2019, where, if you go and get a PET scan, where do you actually have tumor in your body at this point? So, yeah, let me back up for a second because, well, the quick answer is, I had no tumor. There was no tumor anywhere. And to back up is that the Tegristo, this is pre-Kemo, had stopped shrinking

my primary tumor in March of 2018. So this was, you know, almost a year before I began Kemo. And so since they wouldn't surgically operate it to get it out, I had it radiated. Again, I was lucky enough to have a radiation oncologist who worked with me. And I could say I tolerated brain chemo well. The same was not the case to the lung. I had real issues and interestingly enough, we were leaving to hike the Inca Trail and May of that year. So I had had radiation that

we're leaving to hike the Inca Trail and I started having kind of bad chest pain, like a day or two before we hugged the ink 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 on the ink 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 did that successfully. It was great. My eight year old, Tudolin along. You know, she was always the fastest of any of us. We went with our friends and, I mean, 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 of very clean bed and a spa. My middle child, my daughter said to all of the adults, I developed my third eye during that. It was one of those experiences. Like, you don't normally think you're

going to get that out of a, you know, she was, what, 14 at the time. We were all like, what? 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 from Lisbon to Switzerland because I had a conference. I had to go to.

And at that conference, things started to get really bad. I made it through, but not with, again, some funny stories of how I accommodated to it, because I was having crushing pain. Got homes, turns out, of course, I had some rare, I had this rare complication where actually impacted my bones. My radiation oncologist said, the only treatment for this is to put you on long-term opioid therapy. And I was like, oh, no, thanks. I will accommodate. There was 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 NED, no evidence of disease. I like to always say Ned, right? 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 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 Gemsar. And everybody had said all these terrible things about cisplatin and Gemsar was 10 times worse. Everyone was like, you'll be a breeze.

Gemsar is a breeze compared to cisplatin. You are really the exact opposite of everybody, because yeah, I mean, we used to tell patients gems are, it's non-chimo. Yeah, everybody tolerates gems are. I can still remember sitting, because I was 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.

There are nutrients in there, Sarah, that are very good for the plant. That's right. Feel bad about that. It's a very healthy part of the carbon cycle, I'm sure. But I was determined to keep on. I was really close to getting switched to tax all, which I'm like, this is gonna have, that'll be better.

So then had to take another trip 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 because I literally couldn't walk. And I kept thinking to myself, I'm a hypochondriac. This is just because I'm anemic, whatever. I was super short of breath. But I'm like, OK, 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. Everything is mass. My liver, numbers were through the roof. My kidney numbers were high. I had pancidipidia so bad. How anemic were you, Sarah?

I was like six at this point. I mean, it was bad. Really bad. The low six is at this point. Right. And just so the listener understands, the normal would be 13 or 14 of a hemoglobin in your six. So that's really low. And your platelets were how low?

23. Which means you basically don't have the ability to form a single clot. Right, 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 short and subruth with activity, but I was doing okay. And they sent me home. And I was

like, 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? Because I was getting sent home. And they're like, oh my God, we're admitting you right now. So I actually get a backdoor admission to the hospital. And a complete workup starting right then. I had to have a thorescent thesis drained a whole bunch from my lungs.

That was unknown when I got sent home. So you had tons of fluid around your lungs tons of fluid around my lungs It's explaining the shortness of breath. Yeah, and once I was admitted I was promptly transferred to ICU things were going downhill. I had to be put on bi-pap so I had multi-organ failure Had respiratory failure liver failure kidney failure. I was a big failure, okay? Everything was bad. And was this believed to be the result of your body's response to the tumor or the chemo? It was the gyms are. So I got taken care of in the hospital.

I just want to cry to think about the care I got. It was so wonderful. And I just had the best team. I would have died. Nobody can believe that this was well over a year ago now. And I'm healthy with no persistent failures because I was near death. And I was in the ICU for a really long time.

And everyone, every day it went from, I think your kidneys will rebound to 50, 50. They're never going to be normal. I was on plasma frecis, and it turned out I had something called atypical hemolytic uremic syndrome. And to just explain, over 70% of people are either dead or on dialysis right away. It's got an incredible mortality rate. Incredible.

It's incredibly difficult to treat. And so outcomes are your dead or your on-permanent dialysis. So, I was put on a new medication after, you know, going through kidney biopsies, all these kinds of things in the hospital, sent home, did outpatient plasma frecis for a while, and then things miraculously started getting better, right? Not miraculously, it was because of this medication. I was brought. Of course, that meant an infusion every eight weeks, and the worst part to me is it meant no one would put me back on chemo.

Just they wouldn't put you on gems, or they wouldn't put you on anything. Wouldn't put me on anything. And to me, that was devastating because I said, well, kidney failure is one thing, but having this cancer that we know come back is another. So, that was another hard pill to swallow. And long story short, I got better. I went to pharmacogenetics, which is where they actually take a look at what your genetic profile is in response to different drugs.

And it turns out I had a genetic mutation. Hey, I have lots of them. It turns out I had a genetic mutation that didn't allow the gems are to break down. So I was getting toxic doses of this. And I was on a very low dose, but the thing is that I couldn't get rid of it. So normally, if you see a typical hemolytic uremic syndrome with gems are, it's after months and months of treatment. And I got this within four weeks.

Why? Because I was getting mega doses of it, because my body couldn't get rid of it due to this mutation, because of the explanation. And they said, there's no reason you can't take any other chemo. This is very specific to Jemzar. But that was that, sitting weight mode, back to sitting weight mode. And it took another year, but the cancer came back in September of 2020. But the cancer came back in September of 2020. And here's my story from that,

which really made me so determined to work even harder for health equity. Here I am a physician able to grasp really difficult concepts, able to read and scour the literature and know what I'm a physician, able to grasp really difficult concepts, able to read and scour the literature and know what I'm looking for, able to call at a moment time, you know, any time. Someone to help me sort through something I didn't understand, or help maybe refer me to someone. You know, I had all the resources in the world.

made to someone. I had all the resources in the world. And the reoccurrence was in September, even with all my constant pushing and self-advocacy. The one thing is I had, by the time I was diagnosed with cancer, I was an expert, patient advocate, expert, hardcore. And, you know, one of the other advantages I had is it didn't take much to switch that and to become a self-advocate, an advocate for myself. So I was diagnosed in mid-September with a reoccurrence. I did not get on a clinical trial until I got started December 30th. That's a four month delay. That's a four month delay.

For me, an in hindsight, now looking back, before I was panicked, right? And I couldn't really, I was like, something has to get done, something has to get done, something has to get done. I can look back in hindsight and say, how many people die during that time? How many people who don't have the advantages I had just die during that delay. How many?

I shudder and I just wanna cry. And what I've done is I've reached out to other cancer patients to say, has anyone else been in this situation? And I find out it happens all of the time. It seems that we have a really good system, as I experienced, when someone is diagnosed with cancer, they get a health nap, a cancer navigator, you know, they get all these things and we're boom, boom, boom, boom, boom, but when that cancer comes back, it's kind of like

the system seems to give up on you. I had to advocate, advocate the heck out of getting a biopsy done. A biopsy that would be enough tissue to make me eligible for a clinical trial. That would actually get me a full genomics report. I mean, that wasn't going to happen. I'm telling you I had to get almost obnoxious about it. And the stories that I'm getting from people are the same. Where was the recurrence?

In my right upper lobe. So they had to get you had to get another lung biopsy to do this. And can I ask you another thing, Sarah, what has been, you obviously have health insurance, but I assume that there's been a non-trivial amount of pocket costs as well in the last four years. Oh, yeah. Oh, yeah. Do you have a sense of what the out of pocket cost has been for your care?

Tens of thousands of dollars. Which obviously speaks to another challenge. I don't know if this is still true, but it certainly was true at one point that the greatest source of personal bankruptcy in the United States is healthcare, an inability to pay health care costs. And a cancer diagnosis is so high up there. I would have to believe that cancer is the leading subset of that as well. to believe that cancer is the leading subset of that as well. So now I'm like, especially when I got feedback

that I'm not alone in this, it wasn't just me, you know? And again, I always keep saying in the backdrop of, I am one of the privileged. And I was put in this situation. And the fact of the matter is, by the time the reoccurrence was diagnosed, to the time I finally got treated, I had progressed so much that I had compression in my bronchus,

I couldn't get up a flight of stares without desaturating. I mean, this all just happened. I was in horrible shape, which of course, again, and remember, I'm starting out before my diagnosis in general, I was so healthy, which gives me an advantage in this, which gives me a significant advantage in this. But it goes back to that question of how many people just die? Sarah, you're very realistic about the fact that your time on this earth is less than it should be, right?

A 49 year old, otherwise healthy person who's done all the, you know, not 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. 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? How are you managing that? And 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, 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. 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 going to remember about their mom, being the advocate for other patients. So that in 10 years, when another Sarah Halberg 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. 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, everything outside of my family. Like, I would imagine, 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.

How do you do that? A couple of things. Number one, believe it or not, originally, 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 going to lose, right?

They were what I didn't want to lose. And so it was challenging. And I knew I had overcome that. That was a big motivator for me to not be thinking about that. In thinking in that way, and I'm happy to say I clearly have overcome that, but my kids come first. 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 not getting knocked out by the stressors and bad things in life. You know? I mean bad things happen to

good people. 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 going to 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. Or you can try to turn it into 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 was a question I had to ask myself a long time ago, which is, shouldn't you be a cancer advocate now? 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 going to 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 want to work more again for health equity because it spans both, right? It has to do with both diabetes and cancer, and that is so important. So yeah, how I spend my time is really important. So yeah, how I spend my time is really critical. And I want to say it's not like I'm I don't want to paint the picture that oh my gosh I'm the super

woman. I have a terminal cancer and yay life is great. No. 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, you know, great is hard to think about now.

And some people say, well, I'm so cancer really helped me get a new perspective on life and what I care about. And I'm happy to say, I don't know that I got that, okay? I mean, having cancer 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, I cherished travel and showing my children travel. 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 fundamentally different. It's tough. Sarah, you've said a lot of things that I'm obviously resonate

um And I think we'll resonate with a lot of people so I I want to thank you from the bottom of my heart and Certainly wish you the best thanks Thanks, I appreciate it. It's been great knowing you through this journey as well. You are, as many of your colleagues have undoubtedly told you and we've certainly discussed it behind your back.

You are an inspiration and nobody wants to hear that because nobody wants to be the inspiration. You just want to be the normal person, but you are an inspiration. I just want a be a normal person. Yeah. Well, thank you for setting aside time. 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 in any way, shape

or form. So I have been kind of preparing for this and I'm glad I did it. So thank you for giving me an opportunity to do that and thank you. Thank you for trusting us. Thank you for trusting me in the listeners.