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

00:00:00.000 Welcome to a special episode of The Drive. Today's episode is going to be a rebroadcast

00:00:06.280 from an episode released in May of 2021 in memory of the guest, Dr. Sarah Halbert. This

00:00:11.340 podcast, Sarah and I really talk about two completely different things. In the first

00:00:14.160 half of the podcast, Sarah discusses how she became a believer in the efficacy of carbohydrate

00:00:18.040 restriction and the treatment of type 2 diabetes through her clinical experience. She challenges

00:00:22.840 the common beliefs about the role of dietary fat and carbohydrates on the plasma makeup

00:00:27.200 of fatty acids and triglycerides and also expresses importance in the understanding of the early

00:00:31.880 predictors of metabolic illness. But it's the second half of my conversation with Sarah

00:00:35.980 that I really want to highlight. The second half of this episode is perhaps one of the

00:00:38.860 most emotionally riveting discussions I've had on this podcast. It's one in which Sarah

00:00:43.400 tells the personal story of her own lung cancer diagnosis and her journey through that. Sarah

00:00:48.600 was diagnosed with lung cancer at the end of June of 2017, despite having never smoked and

00:00:54.220 only being in her forties. The time she was diagnosed, she already had stage four metastatic

00:00:59.700 disease. And I'm very sad to say that I just learned yesterday at the time of my recording

00:01:05.620 this introduction that Sarah passed away from a very long battle with lung cancer. For those

00:01:11.800 reasons, I wanted to rebroadcast my conversation with Sarah, as I believe it's something that frankly,

00:01:16.000 everyone would benefit from listening to, even if you've heard it once before. While it was

00:01:20.980 admittedly a very difficult discussion to have with Sarah. And while I can't even imagine how

00:01:27.580 difficult it was for Sarah to have that discussion with me, I feel like it was an enormous privilege.

00:01:34.340 And I think that those of us who knew Sarah will be forever grateful. And I think that many people

00:01:41.000 listening who did not have the privilege of knowing Sarah will still be indebted to her for what she

00:01:46.460 shared in terms of her, her zest for life and the manner in which she fought this disease and didn't

00:01:53.640 really let it rob her of who she was. So without further delay, here's a special rebroadcast in

00:02:02.320 memory of Dr. Sarah Halberg. Welcome to the show. I'm super excited to be speaking with you today.

00:02:09.920 This has the potential to, of course, to be a 10 hour podcast, which it won't be, but I think that

00:02:13.940 speaks to the depth of insight that you've got into so many topics that I actually want to talk

00:02:20.340 about. Thank you. It's great to be here. Well, in thinking long and hard about how to navigate all

00:02:26.760 the threads I want to pull on, I figured we would just start with the nerdiest of all topics,

00:02:30.960 which is something that I know you're so passionate about. And yet I don't think gets nearly enough

00:02:38.180 attention. And that is basically the role of dietary intake of both carbohydrate and fats and

00:02:47.560 the relationship that has on the distribution of fatty acids within the body. So let me just start

00:02:53.360 by asking, like, why is that even of interest to you? Well, it's significant interest because it really

00:02:59.900 hits at one of the things people criticize a low carb, high fat diet about is, oh my goodness,

00:03:08.240 you know, you'll get more fat in your muscles, in your liver, and it's going to lead to increased

00:03:15.180 insulin resistance and thereby default going to lead to increased cardiovascular disease.

00:03:21.180 And we know that a therapeutic carbohydrate restricted diet brings down so many cardiovascular

00:03:29.720 risk biomarkers that we're all used to hearing about. Okay, it decreases triglycerides. Okay,

00:03:36.460 it actually can reverse type 2 diabetes in most cases and certainly significantly improve glycemic

00:03:45.240 control in all. But fatty acids, that's not something that's talked about all that often. And what is

00:03:55.400 talked about all that often is this idea of you are what you eat, right? We hear that still every day.

00:04:02.860 Remember, you are what you eat. And this example of what happens when you consume saturated fat

00:04:10.600 in the matrix of a diet that includes carbohydrate restriction is so against that long, worn-out idea

00:04:23.300 of you are what you eat. And so fatty acids play a critical role. Study after study will show us in

00:04:32.100 cardiovascular risk and in future diabetes risk as well. But again, it's not discussed because fatty

00:04:40.880 acids are confusing, let's face it, okay? And most people would rather just fall back on this idea,

00:04:48.740 you are what you eat, which just really flies counter to what the evidence in the peer-reviewed

00:04:57.380 published literature says. So maybe taking even a greater step back from that, Sarah, what is it

00:05:06.460 that attracted you personally as a physician towards the management of type 2 diabetes? Because,

00:05:13.540 I mean, that's how you and I got to know each other was through a company that you're a big part

00:05:18.640 of called Virta Health, which I'm sure at some point today we will talk about. But what attracted

00:05:24.300 you to this patient population? And how is it that you stumbled upon the idea that there was perhaps

00:05:31.260 another way to treat patients with type 2 diabetes that was not kind of the standard treatment, which was

00:05:39.280 chasing glycemic control with insulin or insulin-increasing drugs?

00:05:45.760 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

00:05:54.120 healthcare system, I probably wouldn't have believed you. So it goes back again to the fact that for a very

00:06:03.400 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

00:06:12.020 that was telling people that the way to fix everything was to eat a low-calorie, low-fat diet.

00:06:19.700 I grew up as a product of the 80s, like so many people, where that was the dogma. There was no other

00:06:26.240 way. And of course, entering into college and grad school, where I got both my bachelor's and master's

00:06:33.880 in exercise physiology, I mean, that's what we were taught. Moving on to med school, you know,

00:06:39.140 reaffirmed once again. So when I went into practice as a primary care physician, I'm board certified in

00:06:47.340 internal medicine, it was more the same. But again, it was so frustrating to me all along the way,

00:06:54.560 really, to be continually giving this advice and then have people show up being worse. I'm not making

00:07:01.820 them healthier. I'm making them or I'm watching them become more unhealthy. And that was depressing.

00:07:09.600 And it was really quickly became just to the point where it was like, I can't continue on with primary

00:07:16.500 care for the rest of my life because I felt like a legal drug dealer. I got really lucky here. Okay.

00:07:23.800 I like to say a lot of my pivots are pivoted on anger, right? Pivots in my career. And I was really

00:07:30.540 angry at what was happening on the primary care level. And as luck would have it at Indiana University

00:07:36.640 Health, they knew about my background, knew about my past work in obesity care and asked me to start

00:07:43.440 a program, obesity program. And I jumped at the opportunity. And I was lucky to be able to take

00:07:50.440 some time off over the next year, spend time figuring out what was this going to look like?

00:07:56.320 How are we going to tackle the untackleable, if you will, problem? You know, that is obesity.

00:08:03.420 And I started sticking my nose in the literature, which is something that every physician wants to

00:08:09.780 do, but not every physician is afforded the time. Let's face it. You know, we are just boom,

00:08:17.620 boom, boom, see patients. There's just such a busy lifestyle in everything right now. But I was

00:08:23.380 given a chance to step back some. So I had time to prepare for this. And in that, I discovered

00:08:30.680 carbohydrate restriction as a means to weight loss initially. Listened to some lectures by Dr. Steve

00:08:38.700 Finney and Jeff Fulick. And I was like, whoa, that makes total physiologic sense. And so boy, did I dig

00:08:47.460 deeper into this? I read everything I could get my hands on and really came to the conclusion, which

00:08:55.140 required a lot of cognitive dissonance overcoming, that what I had been saying for well over a decade

00:09:04.120 to so many people was really not founded on good science. And that the field of carbohydrate

00:09:12.460 restriction, while still relatively in its infancy at the time, showed much more promise. And so we

00:09:21.280 opened the clinic as a carbohydrate restricted clinic. But the fact of the matter is, although

00:09:27.660 people were losing weight, what we were seeing that was so much more meaningful was that people's

00:09:34.240 diabetes was like going away. They were having normal blood sugar. We were pulling them off of insulin

00:09:40.480 at rates that I could never have believed had I not been the physician who was taking care of these

00:09:47.920 patients. I was astronomical. Hundreds of units of insulin. First of all, there's two questions I

00:09:53.400 guess I want to ask you. One, were these patients primarily patients with type 2 diabetes or was it

00:09:57.620 primarily obesity of which a subset had diabetes? And secondly, how much resistance did you have in your

00:10:03.540 own institution when you showed up and said, hey, I know you guys brought me in to do this thing. I'm

00:10:08.860 going to do it. But oh, by the way, my secret sauce is going to be this, at the time, very unconventional

00:10:14.160 approach. As you probably can imagine, when patients come into an obesity clinic, most all of them, if not

00:10:22.000 all of them, have some form of metabolic disease. The biggest being type 2 diabetes. So we were seeing

00:10:29.020 type 2 diabetes all of the time, consistently daily. And you're right. I had to take precautions.

00:10:36.600 Because again, this was 10 years ago. And not as much about carbohydrate restriction was known at

00:10:45.760 that time, certainly among general practicing physicians in any discipline, really. And so I knew

00:10:53.100 that I had a head off the potential resistance that was going to come. There was just no question of it.

00:10:59.500 So I actually went about and spent an entire summer meeting with all the departments in our local

00:11:08.940 med center and giving them a 15-minute slide presentation of when your patient comes back,

00:11:17.020 says that Dr. Hallberg told them to eat a lot of fat and not a lot of carbohydrates,

00:11:22.000 that I wasn't crazy, that this was actually based on evidence. And here it was.

00:11:27.220 And you know, Peter, you'd be surprised. I didn't get any pushback. I actually pushed it even to the

00:11:34.180 next level. I was part at that time of the Ambulatory Quality Committee at our institution.

00:11:40.580 And I actually brought up an amendment that all patients with metabolic disease should at least be

00:11:48.240 provided the option of trying this if they wanted. And it passed unanimously. I mean, people got it.

00:11:57.080 Once they had time to pause, take a look at the physiology behind this and realize, okay, yeah, that makes

00:12:02.980 a lot of sense. So it changed my life, right? And again, I like to always say my career is built of

00:12:11.380 inflection points of anger. And as we were seeing these huge changes of diabetes and patients just resolving

00:12:20.340 their diabetes, I became really angry because I was like, where is this? Where's this in the

00:12:26.020 guidelines? How come I've never heard of this before? I mean, this is, I mean, I hate to be like

00:12:31.720 overdramatic, but it truly is quite miraculous for a disease that everyone thought was chronic and

00:12:37.840 progressive. To see people recover from it is quite astounding. And so I decided that I needed to get

00:12:47.080 into research. So actually to start off with, I called Purdue University's nutrition program

00:12:54.200 and asked one of the researchers there if they wanted to help me on just an early unfunded pilot

00:13:00.340 study to prove my point. Looking at metabolic improvements and looking at financial improvements

00:13:06.080 too, because obviously if people weren't taking all this medicine, they weren't costing themselves and

00:13:13.460 of course the healthcare system as a whole as much money. So I talked about that study, presented it at

00:13:19.800 the National Lipid Association quite a long time ago, talked about it actually in my TED Talk, and then was

00:13:28.100 speaking at the Obesity Medicine Association quite a long time ago and actually met Dr. Steve Finney.

00:13:37.180 And that really changed the course of my life as well.

00:13:40.740 So all this time you're sort of putting into practice what Steve and Jeff had been writing about

00:13:46.900 for a long time. And obviously Steve is someone I've been dying to have on the podcast and we were

00:13:52.720 actually supposed to do it at one point in time and then scheduling got in the way. But I didn't

00:13:58.300 realize that you had already sort of gone down this path and yet hadn't actually met him because I took

00:14:03.840 the opposite approach, which was when I started kind of implementing some of these treatments, I'm just

00:14:09.080 a bull in a china shop. I just reached out to Steve right away. I might have been one of the first people

00:14:13.720 to get a copy of the book that he and Jeff wrote in 2011. I think I got a preprint of that book, which I

00:14:19.960 still have, by the way, the art and science book, which I have. It might have more highlights and post-its in

00:14:24.880 it than any book I own. Because I think like you, I was kind of going through the, this can't be. There's something

00:14:32.300 so counterintuitive to this that I, I need to read this over and over and over. I'm going to make sure

00:14:36.560 I get it. So it's funny that that's the case. Now, tell me, where did, you know, were you at this time

00:14:41.360 going to ADA meetings, the American Diabetes Association meetings? And when you would discuss

00:14:46.900 what you were seeing in your practice with your peers who were also on the front lines, taking a more

00:14:52.940 traditional approach, how is your experience being, how was that met? Well, it's interesting. If I was

00:15:00.760 speaking with someone who took care of obesity patients for obesity, they were totally, I get it.

00:15:13.060 I'm doing the same thing to some varying degree. But when you moved out of that space to other

00:15:19.640 sub-specialists, the first thing was, oh yeah, their diabetes will go away, but you're going to

00:15:26.520 kill them with heart disease, right? Or, oh, you know, we all know it works. I'll never forget

00:15:33.160 one of the leaders in the endocrine movement said, look, we all know it works. This is not a secret,

00:15:39.000 but nobody can stay with it. And I was like, you know, I don't know. Here in my practice,

00:15:45.000 I have thousands of patients that would beg to differ with that. And so, you know, those are the

00:15:51.100 feedback that I got. And one of the things was, I knew that there had to be even more research done.

00:15:56.660 I mean, you know, we had wonderful pioneers in Steve and Jeff and Eric from Duke, Westman,

00:16:04.820 but we needed even more. They needed to be larger trials. They needed to really specifically focus

00:16:10.300 on patients with type 2 diabetes because I was convinced almost from the get-go that that is

00:16:16.280 the target population here because that's where we see the biggest improvements. So this chance

00:16:23.040 meeting with Steve at Obesity Medicine Association conference led to a dinner and led to funding of

00:16:32.080 the large clinical trial that we're actually wrapping up in the next couple of months. Right now,

00:16:38.440 we're at the tail end of our five-year data collection of the longest and largest trial

00:16:44.560 looking at nutritional ketosis as a means of reversing type 2 diabetes and prediabetes,

00:16:52.500 which I'll just kind of stick in really quick here. Today actually happens to be the day that

00:16:58.840 the prediabetes paper was published. So I'm really proud to say this is the eighth paper already that's

00:17:06.340 come out of this large trial started by a chance encounter at a conference. We haven't published

00:17:14.020 the prediabetes results until today. So this was a paper that looks at the first two years of

00:17:20.920 prediabetes utilizing a remote continuous support to help patients adhere to a diet aimed at nutritional

00:17:31.120 ketosis. And Sarah, these are patients defined as prediabetic by hemoglobin A1c? Correct.

00:17:39.160 And that's being defined as 5.7 to 6.4? Is that the range? That's correct. Yes. Okay. Tell people

00:17:46.860 what that means. I think most people are aware of what a hemoglobin A1c is, but what does that translate

00:17:52.700 to in an average glucose approximately? Yeah. So we really start to get, for example, fasting. That's the

00:17:58.880 one most people are familiar with. And once you get a fasting glucose over 110, you know, that's the

00:18:05.580 worrisome prediabetes range. And I do have to say here, though, that doesn't mean normal glucoses are

00:18:14.320 okay for everyone. And I think you've had, you know, many people on here talking about the perils of

00:18:21.000 insulin resistance and how it starts to cause significant problems in people who still have normal

00:18:28.400 blood sugars. And I just think that's such an important point and can't be overstated again.

00:18:33.660 But in this study, we're looking at people who had insulin resistance long enough that their pancreas

00:18:42.140 and the beta cells could not keep up with the insulin that was needed to keep blood sugar normal.

00:18:48.560 And their blood sugar started to rise, not yet to the level where a diagnosis of type 2 diabetes could

00:18:57.900 be made. But once again, where we see the impact of insulin resistance affecting the body's ability

00:19:07.620 to keep blood sugar normal due to pancreas being overworked for far too long.

00:19:15.720 And if we believe that, I mean, I don't know what the latest numbers are, but I'm guessing

00:19:20.760 it's still about 10% of the U.S. population has type 2 diabetes. Is that approximately correct? Or is

00:19:26.700 it, are we more than 10% now? Approximately, with also the caveat of much more concerning levels in

00:19:34.360 different minority populations, which of course, hopefully we'll get a chance to talk about later,

00:19:40.980 is just a huge goal with improving health equity in this country.

00:19:47.020 So if it's 10% in all comers, do you have a sense of what it is in Hispanic and African-American

00:19:51.980 populations?

00:19:53.240 Yeah, it gets even higher. It's well into the teens in those and Pacific Islanders as well.

00:19:58.840 So these are populations that, you know, we need to be paying attention, of course, to everyone who

00:20:03.400 has type 2 diabetes. But we also need to be paying attention to who's at greater risk.

00:20:09.340 So what percentage of the population do we believe is formally in the pre-diabetic camp? Which again,

00:20:16.720 I think what you said a moment ago is very important for people to understand. If we go back to the

00:20:20.700 podcast with Jerry Shulman, which is one of my favorite discussions ever on the topic of insulin

00:20:25.740 resistance. I mean, Jerry really laid out elegantly the long time course of this disease. And even if

00:20:33.480 you have normal fasting glucose and fasting insulin, but that early sign of elevated postprandial

00:20:40.500 insulin is really that early sign of insulin resistance that will then lead to postprandial

00:20:45.700 glucose elevations. And even that can still exist in the presence of normal fasting glucose. So to your

00:20:52.900 point, by the time someone registers as a pre-diabetic, quote unquote, I mean, this has been a process that's

00:21:00.120 been going on for five to 10 years. What is our belief about how many or what percentage of

00:21:04.760 Americans, just to make it American-centric for a moment, what percentage of Americans are in that

00:21:09.340 bucket? Well, I tell you, recent studies will show us that over 50% of Americans, adult Americans,

00:21:16.140 have diabetes or pre-diabetes. And a study released a couple of years ago, and I mean, this should shock

00:21:24.700 everyone to its core, based on NHANES data, that 88% of Americans are not in optimal metabolic health.

00:21:38.780 I mean, let me say that again. 88% of adult Americans are not in optimal metabolic health. And that is by

00:21:43.860 looking at NHANES data and taking a look at the criteria for metabolic syndrome. And so the 12% are

00:21:52.700 those who didn't meet any of the criteria for metabolic syndrome. I mean, that's frightening.

00:21:58.160 Yeah. So I was going to ask you if that's exactly what it meant. So just let's state for the listener

00:22:02.960 what metabolic syndrome is. We've certainly discussed it on this podcast, but it would be great to remind

00:22:07.700 people, what are those 12% doing? They have none of the following five, right? They have normal blood

00:22:15.220 pressure, though they do not have elevated blood pressure. And they're not on medication.

00:22:18.720 And they're not taking medication to lower blood pressure. And normal is now being much more

00:22:23.060 stringently defined. But I believe the latest CDC definition of normal is less than 130 over 80. In our

00:22:31.000 practice, we advocate less than 120 over 80. They have normal fasting glucose, and that's defined as less

00:22:38.880 than 100. They have normal triglycerides, which are being defined as less than 150. We argue in our

00:22:46.200 practice, that's very high. And anything over 100 is elevated. They have normal HDL cholesterol,

00:22:53.480 which for men is defined as greater than 40 milligrams per deciliter. For women, greater than

00:22:58.360 50 milligrams per deciliter. And they do not have truncal obesity. And I forget, I think for men,

00:23:05.480 that's defined as 40 inches of waist circumference and women 36. I don't know if that's still the latest.

00:23:11.220 Well, yeah. And I will also point out one really important thing here when it comes to waist

00:23:18.060 circumference too, and the definition of metabolic syndrome. And it little bit goes back to what I was

00:23:23.940 saying before about the consideration of minorities and different ethnic populations, which is we have to

00:23:33.340 take that into account, even when we're defining metabolic syndrome. Because for Southeast Asians,

00:23:43.340 they are defined as having metabolic syndrome at a much lower waist circumference. And for African

00:23:50.940 Americans, we need to really consider as well, because they tend, even in the face of having insulin

00:23:58.380 resistance, they tend to have normal triglycerides and HDL. And so again, we can't be treating everybody

00:24:07.820 the same, but we often do. Yeah, I'm glad you pointed that out. I still remember, it was about 10 years

00:24:15.580 ago when I learned that lesson, which was taking care of an African American patient who had about the

00:24:23.420 most uncontrolled diabetes I'd ever seen. Hemoglobin A1c of 14%. This is a person who's basically going

00:24:30.440 to have their limbs amputated in the next hour. Triglycerides of 89. Just, yeah, just totally

00:24:37.840 normal. You look at their lipid panel, you wouldn't think anything is wrong. Right. And so that's the

00:24:42.780 thing is they can get missed. And so knowing this and educating people on things like this, again,

00:24:48.940 goes back to our working on health equities. And it's so important and so often not something people

00:24:56.440 take into account. And just going back to prediabetes, the most frustrating thing, I shouldn't say that,

00:25:03.880 it's one of the most frustrating things. There are many things about our healthcare system I could

00:25:08.260 enter into the most frustrating. But one of them is patients coming in to see me whose lab showed

00:25:16.500 prediabetes. And I said, oh, you have prediabetes. Oh, no, no, no. My physician said I was fine.

00:25:23.140 The fact that we don't appreciate that by the time you get to prediabetes,

00:25:28.400 there's some really serious things going on here. Their vision is being impacted. Their nerves are

00:25:35.300 being impacted. You know, these are things we can't just say, oh, they haven't, they haven't gotten

00:25:41.160 bad enough to bother with because they're not at the criteria for type 2 diabetes yet. I mean,

00:25:48.200 we have to pay attention. And so that's one thing. If there's any physicians listening,

00:25:54.640 which I know that there are, don't ignore any elevation in blood sugar. That means there's

00:26:01.800 been a problem for a long time already. And patients should be also hypervigilant about this. I mean,

00:26:07.820 I've seen patients in that prediabetic camp, and this is using an example of a male patient,

00:26:14.060 when their insulin sensitivity is restored and their blood glucose comes down by an average of 10

00:26:19.580 milligrams per deciliter, they'll say, wow, I have better erections all of a sudden. And that speaks

00:26:25.240 to even the microvascular damage that's being done long before you get to diabetes. You know, I actually

00:26:30.180 was exchanging emails with a really good ophthalmologist recently and kind of trying to ask how far are

00:26:37.740 we away from being able to use retinal imaging as a screening tool for early, early, early

00:26:46.580 microvascular disease. Because I think the hemoglobin A1C is just far too crude a metric for

00:26:51.200 this. And I actually have seen some interesting literature, and I'm sure you've seen even more

00:26:56.160 of it, that suggests that this is, you know, if you look at the microvasculature in the eye, it might be

00:27:01.420 one of the earliest warning signs of when things go awry. And so in an ideal world, I would love it

00:27:08.040 if, you know, we had tech that basically allowed for quick and easy evaluation of that. So that to

00:27:15.280 your point, it doesn't really matter if your trigs are up or down and your waste is big or not. Like,

00:27:20.980 let's look at the actual place where the damage is taking place and make the assessment on an

00:27:25.980 individualized basis, as opposed to using these sort of population-based metrics, which move in the

00:27:30.720 right direction, but for any one individual can be quite misleading. Yeah. And then I love the eye

00:27:36.600 discussion because, you know, one of the other, I think, really important questions is, once we do

00:27:41.820 get to damage, can we make it better? Can we make it better without, and skip some of the horrors of

00:27:50.340 having diabetic eye disease for millions of patients? I mean, that is a really burning question

00:27:59.660 for me and one that I think we need to really explore. Yeah, indeed. So with that background,

00:28:09.760 let's kind of dive into some of this nerdy, nerdy fatty acid stuff. And I got to tell you, I find this

00:28:16.920 stuff really interesting in part because I think it's complicated enough to make sense of just the

00:28:27.400 eating side of this stuff. In other words, I think people that have listened to this podcast,

00:28:31.900 we've done a number of shows that have dealt with fatty acids. People probably understand that there

00:28:36.500 are saturated fats, monounsaturated fats, and polyunsaturated fats. The saturated fats have no

00:28:43.160 double bonds. So that means every carbon is fully saturated with hydrogen. The monounsaturateds have

00:28:49.740 one and only one unsaturation. So one double bond. And then the polys have at least two of these

00:28:58.120 double bonds. But it's the manner in which these things can be made from each other that becomes

00:29:04.160 quite interesting, isn't it? It's really the way that you can ingest one form and it can be turned

00:29:09.920 into another. So I'm wondering if the easiest place to begin this discussion is to introduce

00:29:17.860 what the fate of a very common fat in our body is, which is the C16 saturated fat. So can you talk

00:29:30.620 a little bit about how abundant that is and what our body's options are for it? What it's called?

00:29:36.460 Let's start with the nomenclature. What does pure C16 look like?

00:29:39.920 That's palmitolytic acid. So it's really interesting what happens. And do you mind if I jump on and

00:29:46.820 share screen here so we can talk a little bit more about it?

00:29:50.900 Yeah, that would make it easier for everybody, I'm sure.

00:29:52.920 I want to start by talking about saturated fatty acids in general. And what we know is that going back

00:30:03.140 here to the basics and looking at the liver. When we have incorporation of saturated fatty acids

00:30:10.760 into our triglycerides, that is correlated with insulin resistance and adiposity, likely reflecting

00:30:19.160 accelerated hepatic de novo lipogenesis. Or also it can be what is actually returned to the liver. So

00:30:27.500 we know really two. We certainly know that hepatic de novo lipogenesis is a big part of the problem

00:30:35.620 when it comes to elevated triglycerides. But we can also make these with some what is delivered exactly

00:30:43.740 back to the liver. And so when we see saturated fatty acids as a makeup of triglycerides or maybe even

00:30:53.500 the phospholipids there, we say, oh my goodness, that's a marker of increased saturated fatty acid

00:31:01.720 consumption, right? These people are eating a high saturated fat diet. And that seems to make sense.

00:31:09.080 And this is the problem with a lot of things in science in general, and nutrition science is no

00:31:15.240 different, is that just because it seems to make sense doesn't mean it's the way things actually work.

00:31:22.620 Sarah, can I explain a technical point on this slide that you and I will take for granted,

00:31:27.880 but I want to make sure that a listener understands. So when a patient goes and gets their blood drawn,

00:31:34.080 let's just say they get a standard lipid panel. It will spit out the following values. Total

00:31:40.060 cholesterol equals 200 milligrams per deciliter. LDL cholesterol equals, you know, 140 milligrams per

00:31:48.180 deciliter. Triglycerides equal 150 milligrams per deciliter. HDL cholesterol is 35 milligrams per

00:31:55.340 deciliter. And VLDL cholesterol, if I remember the numbers I just spit out, would be 25 milligrams per

00:32:01.420 deciliter. In other words, the VLDL cholesterol, HDL cholesterol, and LDL cholesterol sum to the total,

00:32:07.400 and then the triglycerides are independent. What I want to make sure people understand is

00:32:11.820 those are all found within the lipoproteins. So VLDL cholesterol is the amount of cholesterol

00:32:22.320 ester contained within the very low density lipoprotein. LDL cholesterol is the total content

00:32:28.520 of cholesterol ester found within the low density lipoprotein, etc. for the HDL. Here's the part that's

00:32:35.760 really interesting. We always check these things fasting because when it comes to measuring the

00:32:41.500 triglyceride, we want to eliminate what's in the chylomicron. We want to eliminate the immediately

00:32:47.020 absorbed triglyceride from the gut. And by doing that, we basically capture what you have on this

00:32:53.940 photo. When we measure a triglyceride, for all intents and purposes, we are basically measuring

00:33:01.040 the 90% of triglycerides that are captured within the VLDL. So let me restate that because that was a bit

00:33:07.500 rambling. When you go to the doctor and get your blood tested and it says your triglycerides are

00:33:12.620 150 milligrams per deciliter, that's basically saying, look, 90% of that 150 milligrams per

00:33:18.960 deciliter is within your VLDL cholesterol. Some of that is in intermediate density lipoprotein,

00:33:24.760 but that's virtually non-existent. There's a trace of that in the LDL cholesterol and even a smaller trace

00:33:30.480 in the HDL, but the lion's share is in the VLDL cholesterol. And as you're going to explain to us,

00:33:37.860 this process of de novo lipogenesis, the conduit from fat being made in the liver and exported,

00:33:45.000 that conduit is the VLDL particle. That's going to become very important in this discussion.

00:33:49.840 Absolutely. Yeah. And that's really important. Thank you for the precursor explanation because

00:33:54.900 this is technical stuff and that is really important for people to understand. Then the

00:34:01.460 next question really becomes, okay, so if we have a high saturated fatty acid content within the VLDL,

00:34:12.880 okay, again, it's being in the triglycerides, the phospholipid membrane, wherever we find it,

00:34:20.920 where did the saturated fatty acids come from? Is it directly from consumption? And I just want to

00:34:31.040 first point out before we get into maybe more of the technical stuff, some of the clinical trials

00:34:37.040 that can help us understand this a little bit better. And so this is one of my favorites by Dr.

00:34:44.760 Brittany Volk that was published a while ago. And it's really great because this was a

00:34:50.840 feeding study. So, you know, they kept track of what the patients were eating. It wasn't a free for

00:34:56.720 all. Are they eating what they were telling them to eat or not? They provided all of their food.

00:35:04.100 And this was patients with metabolic syndrome. They went through six feeding phases. And so they did a

00:35:12.200 run in with a very low carbohydrate diet for everyone, less than 50 grams of carbohydrates a day.

00:35:19.000 And every three weeks, they increased the carbohydrates in the diet, all the way up to

00:35:27.020 346 grams, which was C6 feeding phase. The other thing to note here is the saturated fat content.

00:35:36.920 So when we were at the low carbohydrate end here in C1, they were consuming 84 grams of saturated fatty

00:35:45.840 acids a day. Okay. So that blows away any guideline on saturated fat. I mean, so far above what anyone

00:35:55.100 would consider at goal. And then we get down to the C6 and we're much less 32 grams. Again, what happens

00:36:05.020 to the fatty acids as people are run through these six phases?

00:36:10.360 And Sarah, just to be clear, this is basically an isocaloric feeding study, which means as you're

00:36:18.280 ratcheting up the content of carbohydrate, you're commensurately reducing at a caloric level,

00:36:27.660 the amount of saturated fat, right? I believe this study did not change the number of calories they

00:36:32.560 were consuming. Correct. They did not. And so what happened over these six phases? So here we have

00:36:42.000 saturated fatty acid levels marked. Okay. So here's the baseline at that run in. And we see when we have

00:36:50.380 the very high saturated fat level, very low carbohydrate. Here we go. And what's really

00:36:58.040 interesting is what happens as we march along here down to C6. And if you remember, this is much

00:37:05.600 lower saturated fatty acid content of the diet, much higher carbohydrate intake. What we see is that

00:37:16.160 it's actually the saturated fatty acid content is actually higher with the lower saturated fat intake.

00:37:25.060 And we're going to come back and talk to about the science behind that. But I think it's really

00:37:29.760 important for people to see this clinically. And then maybe when we get into a little bit more of

00:37:35.400 the nitty gritty, it can make more sense. I mean, it's actually statistically insignificant

00:37:40.900 in terms of C16, right, which is the dominant saturated fatty acid. So palmitic acid, it trended

00:37:49.860 towards an increase as dietary saturated fat went down and carbohydrate went up, but it didn't reach

00:37:58.860 significance. And the only one that actually did significantly increase was C14, right?

00:38:06.800 Yeah. Actually, C16 won as well. And that one is we're going to spend hopefully a little bit of time

00:38:13.560 on. Yeah, yeah, yeah. No, but as a saturated fat, it was really just... Oh, as a saturated fat. Yes.

00:38:18.160 Yeah, yeah, yeah. But the point of this is we didn't have these really high levels of serum

00:38:26.300 saturated fatty acids when we were consuming, when these participants were consuming this

00:38:32.120 very high saturated fat diet. Essentially, and this is important, it stays the same. If anything,

00:38:40.420 there's a trend to higher serum saturated fat in the low fat arm, okay, but certainly we do not see

00:38:52.320 a rise in the high intake of saturated fat. That's super important. And again, it goes against what I

00:39:01.120 was saying earlier on. You are what you eat. Well, okay, if that's true, then when I consume a very high

00:39:09.920 level of saturated fatty acids, why am I not seeing that again in the blood, in the serum? Why are we

00:39:19.560 not seeing that? And what's nice in this study is you've exhaustively looked at where the fatty acids

00:39:28.060 are. So obviously the most efficient place we store fatty acids is in the triglyceride, but you also store

00:39:35.420 it within the cholesterol ester. And it's obviously in the phospholipid as well. But regardless of where

00:39:43.540 you look, you see no association between dietary saturated fat and fatty acid composition with

00:39:52.460 respect to saturated fat. That's right. That's right. And I want to really quick draw attention here

00:39:58.560 to one more that we are going to be talking more about. And that's 16-1. That's palmitaleic acid.

00:40:09.280 And we're going to talk more about why that's important. But as we can see here, when we follow

00:40:15.440 that across, it significantly rises when we have less saturated fat and more carbohydrates. And you can see

00:40:25.000 that is statistically significantly different in every place that we're looking. So moving on,

00:40:34.280 one other trial that shows this, and then we'll bring up the table that I had erroneously brought up

00:40:41.580 for the first study. But when we take here a low saturated fat diet, low fat, low saturated fat diet,

00:40:49.780 and we compare it to a low carbohydrate, high saturated fat diet over 12 weeks. This is from

00:40:58.560 Jeff Volick's group from 2008. And what I like here is you can see very readily with these pie charts

00:41:05.860 exactly what the content of the two diets were. So again, we really have it flipped. High carbohydrate,

00:41:14.300 low carbohydrate, low fat here on the left to a very high intake of fat on the right. And again,

00:41:23.900 below it, the two different levels of saturated fat that we're comparing. 12 grams to three times as high

00:41:32.460 in the low carb diet at 36. These are both really low calorie studies. Was this an ad lib feeding study

00:41:40.580 or were these deliberately calorie restricted? How was this study done? Yeah, these were both that

00:41:47.040 wanted the calorie intake of the two studies to be the same. So as you can see, they're about 1500

00:41:52.320 calories a piece. And were they deliberately calorie restricted? Yes. So what we can see here

00:41:59.820 is that what we have when we take a look at these two arms is taking a look on the right to the change

00:42:08.600 in serum saturated fatty acids. We can see in the carb restricted diet, significant decrease

00:42:17.000 versus the low fat diet. So again, in the much higher saturated fatty acid arm, we see a significant

00:42:26.220 decrease down. Whereas we do see a drop in the low saturated fatty acid intake group, but not nearly as

00:42:35.060 much as we see with the carbohydrate restricted group. Once again, arguing against you are what you

00:42:42.920 eat. And I want to now get in a little bit more to this, what I think is actually even more important,

00:42:50.720 which is the change in the palmitoleic acid. Yeah. So palmitic acid is 16-0. Palmitoleic acid is 16-1.

00:43:00.260 They look almost the same, except that palmitoleic, the 16-1 has that double bond at the N7 position.

00:43:09.720 And you're going to explain in a moment which enzyme does that and why that matters, right?

00:43:15.420 Right. Absolutely. You know, what is it about this? It's not a saturated fatty acid. So why do we care

00:43:21.240 so much? What happens to 16-1? But it's pretty evident here what happens first of all, and then we'll

00:43:28.440 talk about why. What happens is that with 16-1 in the high saturated fatty acid group, it drops

00:43:37.360 significantly. Where in the low fat group, again, low saturated fatty acid group, it actually goes up.

00:43:46.080 And this is a statistically significant difference, okay? Much more significant even as we look than the

00:43:54.140 change in the serum fatty acids. So now I'm going to pull up a graph of these results to look at it a

00:44:02.840 little better. And then I want to get into the actual science of it. This is the very low carbohydrate

00:44:09.780 arm on the left, and it is the low fat arm on the right. And so what we see here, when we look at total

00:44:19.900 saturated fatty acids, is that it has dropped 5% between the low carbohydrate group and the low fat

00:44:32.120 group, total saturated fatty acids. What about the 16-1? And what we see here with the 16-1 in much

00:44:42.820 more significant statistically, is that we see between a low carbohydrate diet and a low fat diet,

00:44:53.460 that we have a more significant decrease in the 16-1 with the low carbohydrate, higher fat diet.

00:45:06.160 So there's a couple things going on here for people that are going to be overwhelmed by this table. And I

00:45:10.640 apologize if you're just listening to this without watching it on video. I'll do my best to explain what's

00:45:15.620 going on here. So the first thing to notice here is both of these groups of patients started out with quite

00:45:21.480 elevated triglycerides. So in the first group, in the group that was randomized to the very low

00:45:28.640 carbohydrate diet, their average triglyceride at the start of this study was 211 milligrams per

00:45:34.440 deciliter. That's sky high. At the end of 12 weeks, it was down to about 104 milligrams per deciliter.

00:45:42.280 It fell by about 50%. Conversely, the group that started out in the low fat arm, also very high

00:45:49.700 triglycerides to start, 187 milligrams per deciliter. By the end of 12 weeks, they saw about a 20% reduction

00:45:56.960 to about 150 milligrams per deciliter. Now this is where these tables get a little bit confusing

00:46:03.320 because the table is showing both the relative and absolute reduction of the relative or

00:46:12.020 constitutive fatty acid. In this case, 16-0 and 16-1 and 7, the two we're talking about. What does

00:46:18.400 that mean in English? It means that when you look at the total amount of saturated fat reduction on a

00:46:25.640 relative basis, both groups saw a slight reduction, but it was statistically more significant in one group

00:46:33.160 than the other. The low carb group was a 12% reduction versus 5% in the low fat group. And on an absolute

00:46:41.260 basis, that difference was even greater because the low carb group had such a significant reduction in total

00:46:48.500 triglyceride as well. And that's the dominant source of where you're going to see these fatty acids. And of course,

00:46:53.900 the reverse is true when it comes to 16-1. So let's now ask the question, Sarah, what is it about

00:47:04.400 palmitolaic acid that you think is such an important biomarker? Because we wouldn't be having this

00:47:10.960 discussion if you didn't think we should be paying attention to this. I think it's a really important

00:47:16.280 biomarker. And if you would allow me, let me point out one other thing here regarding the triglycerides,

00:47:22.520 because clearly the low carbohydrate arm decreased more in the triglycerides. The low fat arm decreased

00:47:31.960 too, which may come as a surprise to your listeners because we do associate low fat with an increase

00:47:40.260 in triglycerides. But I do want to remind everyone that this was a calorie restricted. This was around

00:47:47.340 1500 calories. So that drop in the low fat diet arm, although maybe not what we were expected,

00:47:55.940 does make sense with the reduction in calories overall. Now, let's go back and talk more about

00:48:03.340 your question. Okay. I think palmitolaic acid, or again, that's that 16-1, is really not appreciated

00:48:13.700 as the health predictor that it really is. Okay. So let's go through, I'm going to just jump ahead

00:48:23.800 a little bit here. So palmitolaic, or we like to call it POA, is a product of something called

00:48:32.580 sterol-CoA desaturase. And sterol-CoA desaturase. And sterol-CoA desaturase is going to determine

00:48:41.520 what is going to happen with some of the fatty acids in our system, specifically what's going to

00:48:50.780 happen to POA. Now, what we know ahead is that sterol-CoA desaturase is actually an independent

00:49:00.300 marker of triglyceridemia and abdominal adiposity. So in other words, an independent marker of all

00:49:07.760 those things that go along with insulin resistance. So if we have high levels of sterol-CoA desaturase

00:49:16.560 activity, right there, we got to start thinking things may be concerning, even if someone has

00:49:25.020 a normal blood sugar. Right? Because right now, I think one of the important things based on

00:49:30.840 the earlier part of our conversation, where we say so many times these things are missed,

00:49:36.400 people can still have normal blood sugars, it's going to be really important, you know, number one,

00:49:42.240 that we make everyone aware that a normal blood sugar doesn't mean that you are healthy. But number

00:49:48.320 two, what are some easy ways and some easy markers, maybe that we can check to know that we're headed

00:49:55.180 for trouble, even before we have blood sugar go up. So plasma triglycerides, and let's take a look

00:50:04.520 at, again, POA in those plasma triglycerides, in the way of looking at it in core tiles. So again,

00:50:14.780 low versus high, what we can see is the POA, the byproduct of sterol-CoA desaturase is much higher,

00:50:27.580 the higher the triglycerides are. Very important. So if your triglycerides are really high,

00:50:35.100 again, what's happening very likely is that your POA is elevated as well, brought about by increased

00:50:44.220 activity of sterol-CoA desaturase. And this shouldn't be surprising, right? Because if you look at the

00:50:54.260 very unfriendly diagrams of fatty acid metabolism, one of the first steps we see in the conversion

00:51:03.760 or elongation of fatty acids is the conversion of C-16-0 palmitic acid into C-16-1 palmitoleic acid

00:51:16.340 N7 through an enzyme that has two names, I guess, depending on the name and nomenclature, right? So

00:51:21.700 delta-9 desaturase, desaturate the number nine carbon from the delta end, also known as sterol-CoA

00:51:29.100 desaturase, which I think is the more popular name, is SCD-1, right? Right. And if you go down

00:51:35.180 that pathway, what you're basically doing is bundling and packaging fat to leave the liver,

00:51:41.920 right? Yes. And here is one of the, that is an interesting point because the question is if we're

00:51:49.420 trying to change the serum saturated fats into something else, I mean, the body is obviously doing

00:51:58.680 that. One would have to wonder, is that a protection mechanism? Why do we want to do that?

00:52:06.600 To me, that's a great question, Sarah. It seems counterintuitive if I'm going to be obvious because

00:52:10.760 we would think that a saturated fat is much safer. It's inert. There's no chance a reactive oxygen

00:52:18.080 species can be formed out of it. Why is it our body, even if we wanted to export fat from the liver,

00:52:23.760 which we could argue all the reasons that's not a great idea, why would we go to the trouble of this

00:52:28.620 conversion? All right. Well, let's go through it really quick and then get to answering that

00:52:33.840 question because I think it's really important and really sheds light on why we need to be paying

00:52:40.800 more attention to the all-important POA and, of course, the precursors and enzymes that act in its

00:52:50.600 creation. So let's go through, if you will, this cartoon that I know looks really busy initially,

00:52:56.840 but let me just kind of run through it starting here in the intestine. And remember, we'll start

00:53:04.700 off by saying our focus in healthcare and in nutrition recommendations for so long has been

00:53:11.220 low fat, low fat, more carbohydrates, higher carbohydrates. Well, let's take a look in the

00:53:16.860 intestine at those carbohydrates, changing the focus for a minute. So they come in rapidly absorbed

00:53:24.660 carbohydrates or even our slowly absorbed carbohydrates, our starches, okay? And what happens when they come

00:53:33.080 in? As glucose, that feeds in again through GLUT2 into the pancreas, pushing out more insulin. Insulin then 0.59

00:53:44.060 feeds into the liver. And what we get here is going through a big, big part of this is SREBP1, okay? And I

00:53:56.800 don't know if we need to get that technical, but we'll lead here to that enzyme we were talking about,

00:54:04.240 the SCD1 or sterile coa desaturase, increasing. Very important. And it comes about through other means

00:54:13.680 as well. Fructose coming in through GLUT5 or glucose coming directly into the liver through GLUT2.

00:54:22.300 They're all feeding into this by slightly different mechanisms to increase this SCD1.

00:54:31.800 Now we're going to look more at the process in a different way. So we have increased hepatic, first of all,

00:54:41.760 saturated fat. Okay, here's our 16-0, the saturated fat. Increase hepatic levels of this. What gets

00:54:52.820 turned on as from the past cartoon, we get that SCD1 activity increasing that leads to this increase

00:55:05.640 in POA. Coming down here, what's the end gain here? Increased VLDL. Same thing over here, looking at it

00:55:19.240 different. We see again, SCD1, if it's blocked, we won't see that. We'll see a decrease in VLDL.

00:55:30.780 And this, again, has to do if this SCD enzyme is blocked, we're going to have an increase in the 0.64

00:55:40.060 saturate, a decrease in our POA. But again, what we have when we're consuming the high carbohydrates,

00:55:52.020 even if they're the, again, more refined carbohydrates or the less rapidly absorbed

00:55:59.980 carbohydrates, this is the path that we wind up going on. 16-0, saturated fat is elevated,

00:56:09.060 and it turns on this cascade, leading to increase in VLDL.

00:56:15.900 Yeah. Again, I think for folks that are watching this, it's going to make a bit more sense. And if

00:56:20.540 you're not, I just want to make sure we're bringing you along for the ride. So in the liver,

00:56:25.480 when you are taking C16 or C18, but let's just keep the discussion simple and start with a saturated

00:56:31.460 C16, the first committed step is going through SCD1 as an enzyme, and it adds that double bond.

00:56:39.440 It makes a few more steps along the way, but ultimately, it is increasing a process of

00:56:45.600 lipogenesis. It is making more lipid. It is increasing the amount of lipid within the

00:56:50.900 cholesterol ester and the triglyceride. It is being exported from the liver. So in response to your

00:56:55.780 question, Sarah, is this protective? I guess the answer looks like the body is saying, well, gosh,

00:57:02.100 I would rather get this fat out of the liver than keep it in the liver. And we know that it's not

00:57:06.660 fully successful in doing that because of course, although it hasn't come up yet on this discussion,

00:57:11.880 everything we've talked about today runs hand in hand with non-alcoholic fatty liver disease,

00:57:17.160 which is truly an epidemic at the moment. But I suspect that the body is still doing its best,

00:57:23.500 even in the case of non-alcoholic fatty liver disease, to try to export this fat as much as

00:57:27.860 possible. The triglyceride is a very efficient place to store it. I've always believed obesity

00:57:34.260 obesity is a protective mechanism. I think that obesity is not the cause of metabolic illness,

00:57:40.780 but the result of it, which is not to say that the inflammatory environment that comes with it

00:57:46.020 doesn't pour more gasoline on that fire. But it is my belief that everything we're talking about here

00:57:53.200 is the body's aim to protect itself from an abundance of nutrition. And so that's how I read

00:58:00.240 this is the body is doing, and specifically the liver, which is arguably the most important organ

00:58:05.160 in this situation. And the liver is really trying to protect us. And it's saying, I'm making so much

00:58:11.200 extra fat right now because you as my individual are so far above your carbohydrate consumption

00:58:17.320 tolerance, your tolerance for carbohydrate consumption. And this is the most efficient thing

00:58:21.740 I can do, which is turn that into fat, send it out via the VLDL, get that into the adipose site. And

00:58:29.080 yeah, you're going to be a little bit fatter and it's going to come with some downstream problems,

00:58:33.100 but in the short term, it's protecting me, the liver. Would you agree with my teleologic view of that?

00:58:39.740 I 100% would agree with it. And again, I think that we're going to have more and more details on this

00:58:48.140 coming out very soon in many research projects that are currently ongoing. But what it really comes

00:58:54.140 down to is we want to know what an individual's carbohydrate tolerance is, okay? I mean, that's key

00:59:03.820 to personalization, right? Does everybody need to be very low carbohydrate, low carbohydrate? I mean,

00:59:11.660 where does, we can say population level, what happens in large clinical trials,

00:59:16.860 but what's happening with the individual? Because let's face it, Peter, and you know,

00:59:21.820 you and I as practicing clinicians know this, when you're sitting with one patient in front of you,

00:59:28.140 you can go over group data from a clinical trial. And that's an important part of the decision making,

00:59:34.940 but the only thing that really matters is what's going to happen with the patient right in front of you.

00:59:41.900 We really want to know what the individualized reaction is going to be. We know that this happens

00:59:49.100 with a carbohydrate consumption above a certain threshold, but what that certain threshold is

00:59:56.540 in the individual, we don't know. And based on these pathways, you know, what is the marker we want

01:00:03.500 to be looking at? Actually, it's probably POA, surprisingly not a fatty acid. But what this tells us is that when

01:00:14.620 someone has consumed carbohydrates above their individual tolerance, that POA level is going to be a

01:00:25.260 great biomarker. It's going to go up as, again, a protective mechanism in the liver. Our livers are

01:00:34.460 really, I mean, we talk about livers all the time, so related to insulin resistance. It's just always

01:00:40.300 amazing just how sophisticated and how our livers, although we think of them as producing things that

01:00:47.500 aren't necessarily good for us. And that may be true. They're also really working for us as well.

01:00:54.300 And so again, I want to also go back on one other thing that you said. And the other thing that you

01:01:00.460 said is, so this comes before the adiposity. And I think that that is such an important point. And one,

01:01:09.100 I like to preach every opportunity I can get it. But this is starting to happen before people gain a

01:01:17.660 lot of weight. This is a disease process in and of itself that causes obesity. So we have to really

01:01:28.300 take that into account when we're in the office with someone who's struggling with obesity. And I know,

01:01:34.780 Peter, you take this really to heart, approaching and treating these patients without bias, as I do. But

01:01:41.980 it's so important for other providers to be looking themselves in the mirror and asking themselves,

01:01:48.140 what are the biases I hold against patients who come to me struggling with their weight? And what do I

01:01:55.740 really know about the science? And what it really one must conclude is that this is not their fault.

01:02:04.060 These are things that happened beforehand. And they're suffering the consequences of it. And the

01:02:09.740 problem is the consequence is on full view for everyone to see. It's not something that they can

01:02:16.460 hide. And that makes them so vulnerable to bias in health care. And again, one of the other things I

01:02:23.100 come back to is part of our whole battle in health equity.

01:02:27.420 So Sarah, I want to keep digging into this idea because it's so interesting to me of having a

01:02:32.620 leading indicator for this early, early, early warning sign. We talked about it at the outset of this

01:02:40.060 discussion, which is in some ways the tragedy of using hemoglobin A1C as the marker of when somebody

01:02:47.180 gets on the radar. I mean, you said it yourself, patients will show up and nobody's ringing the

01:02:52.780 bell until their hemoglobin A1C is above 6.5. But that literally is happening 10, 15, maybe 20 years

01:03:01.500 after there were early, early molecular warning signs. And if measuring palmitoleic acid is one of

01:03:08.460 them, that's exactly the kind of stuff that I find interesting because in our practice, we use CGM a lot.

01:03:14.060 So continuous glucose monitoring, non-diabetics are wearing CGM like it's no tomorrow in our practice 1.00

01:03:19.980 because of that exact reason. We're basically holding them to a very high standard of average

01:03:24.580 glucose and high excursions and all these sorts of things. I want to go back to something that you

01:03:29.580 alluded to, which is the association between palmitoleic acid and triglyceride is so tight

01:03:35.820 that would we miss, for example, African-American patients? Do we know if they're failing to synthesize

01:03:43.040 C16-1 in the way a white patient is? Wouldn't we love to know that? There's not been a good trial 1.00

01:03:51.360 looking at that. I mean, one of the problems that we have in research in general is that we tend to

01:03:57.900 focus on white people and actually worse middle or upper middle class white people. So there are a lot

01:04:04.940 of questions with this in specific populations. There have been a couple of studies recently coming

01:04:12.860 out looking specifically at what we're talking about, POA, and its marker for future problems and

01:04:21.020 predictor of future diabetes and other issues. One was a study recently published called the Panic Study,

01:04:29.500 looking at levels in childhood and seeing how they translate to health consequences decades down

01:04:37.140 the road. And then there was another study, I believe it was from the Netherlands, where they

01:04:43.560 looked at POA levels at 50 to correlate them with C-reactive protein levels at age 70. And what we see

01:04:53.280 is what we would expect based on our discussion here, which is the POA was a predictor of problems down

01:05:00.320 the road in people who were healthy when their POA was elevated or healthy, so we thought. What we

01:05:08.580 really want to know ahead of time, and I know this is very meaningful to you in your practice, is I want

01:05:15.320 the person who's healthy so I can get to tell them how to stay healthy. We talk a lot about trying to

01:05:24.400 work on people who are already, so to speak, behind the eight ball, and we want to work them out and we

01:05:29.880 want to regress their disease, clearly an important goal. But we also really, if we're going to make a

01:05:37.580 difference, again, with the individual and population-wide, we need to know who's headed for trouble.

01:05:45.680 Again, I hope there's an ongoing effort here because I think this is the future of medicine,

01:05:50.380 right? I mean, I think the future of medicine has to be coming up with tools that allow us to take

01:05:57.640 broad sweeping population-based insights and very quickly target individuals. And if we have

01:06:05.200 biomarkers like this that can say, look, the moment this is triggered above a certain level, it doesn't

01:06:10.940 really matter what your glucose is and your insulin might still be normal. This is time to

01:06:15.020 intervene. And then, of course, the second part of that equation is what's the right intervention and

01:06:19.060 how do we pair people to the right intervention? Again, you and I have a very similar set of

01:06:24.220 experiences, which is patients with hyperinsulinemia and elevated glucose generally respond well to

01:06:32.560 carbohydrate restriction. My practice also focuses so much on the role of glucose disposal and

01:06:38.160 non-insulin-dependent glucose disposal through exercise. And I know that that's probably not a

01:06:43.600 surprise to many people is sort of correcting the sleep, exercise, nutrition trifecta, and then adding

01:06:50.040 to that the role of cortisol in all of this. So I think this is a very hard problem to solve. That's

01:06:55.300 the bad news. But I think the good news is if you get this one right, you get a leg up on every

01:07:01.560 chronic disease. So your risk of heart disease, cancer, Alzheimer's disease, all go down. And so

01:07:09.480 it's worth this enormous effort to continue pushing on these questions. On that note too, and when we

01:07:16.100 talk about individualization and risk prediction before we're seeing our classic biomarker issues come

01:07:23.480 up, has to do, I'll circle it back to carbohydrate restriction. Because we know very low levels of

01:07:30.940 carbohydrate restriction can reverse the disease process, bring about normal glycemia in patients

01:07:38.800 and be able to get them off of medications. But we could put a risk predictor like POA into wider use,

01:07:45.680 okay, which would give a person their individual carbohydrate threshold. What if it didn't need to be

01:07:52.780 as low? What if we caught them earlier in the disease process and we're like, hey buddy, you go over,

01:07:58.860 you know, 175. That's where trouble comes in. Rather than you need to stay very low indefinitely

01:08:07.180 because we've caught you on the spectrum of the disease so late. And this is what we really need

01:08:14.040 to do to control this, to keep your glucose normal without the use of these many medications,

01:08:21.960 especially insulin. I want to ask you another question on this, Sarah. And again, I don't know

01:08:27.100 if it applies to patients that you've treated with diabetes or those in the pre-diabetes category,

01:08:31.860 but have you treated patients for long enough on ketogenic or very low carbohydrate diets

01:08:38.880 who showed up in a state of metabolic disarray, ran through a lengthy period of this? So maybe spent

01:08:47.280 years on a carbohydrate restricted protocol and everything gets better. So the weight goes along

01:08:54.860 for the ride, but obviously, and more importantly, their metabolic markers improve and they gradually

01:08:59.620 reintroduce some amount of carbohydrate back in the diet. And all of a sudden they're fine.

01:09:04.480 Almost as though you reset them during a long enough period. How often do you see that? And what do you

01:09:11.140 think is the best explanation for that? See it all the time. And the best explanation for it is what is

01:09:16.420 their insulin reserve. So the majority of people can go ahead, starting out even at long-standing diabetes,

01:09:26.080 reverse their disease, get normal glycemia, get off of all their medications, and then slowly reintroduce

01:09:32.980 carbohydrates as long as they have functioning beta cells. Okay? The problem is the longer you've had

01:09:41.240 diabetes clearly is a risk factor for this. And we can, we see evidence of that in the bariatric

01:09:46.440 surgery literature as well. I mean, there's been so many studies looking at beta cells. And the

01:09:52.460 fascinating thing is who is getting back some of their beta cell function? In other words, maybe their

01:09:59.680 beta cells were only dormant and were able to wake them up again versus which are gone and not coming

01:10:08.280 back. I mean, the fact that people were on the incredibly high dose of insulin, okay, starting

01:10:15.920 on a very low carbohydrate diet. And then they got better right away. A lot of the change is swift,

01:10:25.100 but they couldn't get off insulin. And it was just years went by, right? And they're just staying on this

01:10:32.360 much lower level of insulin. And then all of a sudden, they come off of it. I mean, logic would

01:10:39.940 tell us that some sort of beta cell function has returned. It took a long time. Reset the system,

01:10:48.100 help them heal. You know, I mean, we don't completely understand this. There's so many great scientists

01:10:53.780 looking at this right now, but we still don't have a certain answer, you know, because the answers

01:10:58.680 on the personalized level is how many of mine are dormant? How many of mine are dead, right?

01:11:04.340 What's it going to take for me to wake these up? If it's impossible, I'd like to know that because

01:11:09.600 that sets expectations ahead of time, right? You can get a lot better, but there's always going to

01:11:14.780 be a little insulin in your life. It doesn't mean if they are someone who doesn't have any insulin

01:11:22.160 production capacity that they can't get a lot healthier, but they may not ever be able to get

01:11:28.180 off of insulin. And so that's where it gets down once again into that nitty gritty personalization

01:11:33.840 aspect. And wouldn't that be nice to know? But I think that the answer to the larger question is,

01:11:41.660 why is this happening that some people can start to eat carbohydrates? Not anywhere near to where

01:11:48.240 they were, but they're able to put some back into their diets versus people who can't is beta cell

01:11:55.220 function. Something in there that you said is very important that I don't think historically has

01:12:00.560 been communicated well enough to patients, which is that insulin, while an amazing and important

01:12:05.140 hormone is not benign. And there's a big difference between taking a hundred units of insulin a day to

01:12:10.560 achieve normal glycemia and taking 20 units of insulin a day to achieve normal glycemia. And you'll

01:12:16.280 take the latter over the former all day, every day, non-negotiable. And some patients will say,

01:12:22.260 well, gosh, I'm still on insulin. This hasn't worked. And not realizing, no, you've had a five

01:12:26.380 fold reduction in your insulin requirement. That's an enormous improvement in your health outcome.

01:12:32.000 And let's put the economics aside. The economics are enormous, but ignore that for a moment. Just in

01:12:37.340 terms of health outcomes, the negative effects of hyperinsulinemia. I just want to say with that,

01:12:42.640 you know, if we really think about the way we manage diabetes, rather than work to actually reverse

01:12:49.260 the disease process and get people off of medication, I mean, management constantly leads to

01:12:55.040 more and more and more insulin, which we know, I mean, on the outward, the appearance of it is that

01:13:02.080 people gain more weight when they go on more insulin. But, you know, if we really get down to the nuts and

01:13:07.440 bolts, when we take someone with type two diabetes, whose glucose is out of control to the point where we

01:13:13.220 need to put them on insulin, the mandatory discussion that needs to occur is, I'm going to give this

01:13:19.740 medication, this insulin that you're going to inject to you. And I'm going to do that because your blood

01:13:25.500 sugars are so high that they could acutely kill you, put you into the hospital, put you at risk of all

01:13:32.840 these complications. But I just want you to know you're more likely to die on insulin. That's what we

01:13:40.180 need to tell people. That's the truth. And, you know, that would have changed the approach a lot

01:13:46.740 of patients want to take. And it would certainly, if providers were forced to look at it that way,

01:13:53.020 when they're staring each individual person in the face, maybe they would treat it differently as well.

01:13:59.380 Yeah, I agree. So I want to talk about something that has been such a big part of your life in the

01:14:06.140 last few years. And people who don't know you may be almost surprised at where we're going in this

01:14:11.260 discussion now. But, you know, this discussion could basically continue down the path. If we

01:14:15.960 could talk more about diabetes, we could end this discussion here. And people would say, wow, that's

01:14:19.980 a really insightful, thoughtful person. But there's a whole other side to your experience with

01:14:25.220 healthcare, Sarah, that started, gosh, almost four years ago. I'll tell the beginning of the story

01:14:29.880 just from my end. So you and I obviously met each other through Virta, your early part of the

01:14:36.900 creation of this company, which is basically scaling up a way to remotely treat patients with type 2

01:14:44.000 diabetes. This is a company that Steve Finney is also a co-founder of, along with Jeff Olick,

01:14:49.000 I believe. I have a minimal involvement in that company. I'm a small investor and at one point was

01:14:54.940 an advisor. But it was during one of these advisory meetings that you and I happened to be sitting next

01:15:00.520 to each other. Now we'd met many times before that, but I do remember this very well. It was,

01:15:04.400 I think, June of 2017. It was up in San Francisco, a large U-shaped table in the room. And, you know,

01:15:12.020 it was a two-day ordeal and you were sitting to my left and that gave us more time than most times to

01:15:18.520 be chatting about this, that, and the other thing. And you looked in perfect health as always. And

01:15:23.280 at the end of the second day, I said goodbye and see you next time and blah, blah, blah, blah, blah.

01:15:28.700 And then about a month later, I heard from a mutual friend that you had been diagnosed with lung cancer

01:15:34.820 and I just about fell off my chair. So can you tell people what happened that summer,

01:15:41.280 the summer of 2017? Yeah. So I'll just start by saying I've been someone who's taken care of

01:15:48.820 themselves to the max all my life. Eating well, I've kept my weight at a normal weight. Even nine

01:15:57.680 months pregnant, I would have still been considered normal weight. Exercise like crazy, competed in,

01:16:03.020 you know, half marathons, triathlons, Olympic distance. I did everything right. Never smoked,

01:16:10.140 never drank to excess. And it was June 30th. So right after that, it was June 30th of 2017. I was

01:16:19.760 having a normal day. I was, went to exercise. I had a big IRB meeting in the morning, went home due to my

01:16:28.640 wonderfully full house of three kids and took a business call in the basement. Cause that's was,

01:16:35.680 that's always my escape place where it can be a little less noisy. And all of a sudden I couldn't

01:16:41.260 talk and I, I couldn't figure out what was going on. I knew something wasn't right, but I couldn't

01:16:47.420 speak. And all I know is that I hung up the phone at some point cause I was embarrassed. I was, remember

01:16:54.940 thinking there, he's going to think I'm drunk. The next thing I remember was being in the car with my

01:17:03.460 husband and him saying, I don't think we could take you to urgent care. I have just very flashes of

01:17:09.280 this day. And the next memory is in the trauma bay at the hospital, the hospital that I work at,

01:17:18.600 where I had seen patients many, many times. And I'll have to tell you the other thing is the last time

01:17:24.540 I had been in that particular trauma bay was when I brought my then four-year-old daughter

01:17:29.840 in, or my husband did. I met them via an ambulance after a traumatic brain injury.

01:17:36.660 So it was like a very bad place for me, although my daughter completely recovered.

01:17:43.300 And I remember screaming at my husband that they're wrong, they're wrong. And I wanted to see the

01:17:49.200 computer because what had happened when they first came in is they thought it was a stroke. And so my

01:17:55.860 poor husband was all of a sudden tasked with, you know, are you going to give her clot busting 0.99

01:18:01.440 medication or not? Because we think she's having a stroke. But lo and behold, the imaging showed

01:18:07.540 a really large tumor in my brain. Then they imaged the rest of me and it turns out I had multiple

01:18:15.740 tumors in my chest. And so they presumed, you know, correctly at that point that this was lung cancer,

01:18:23.380 but I also needed emergency brain surgery. I remember most of this by people telling me about

01:18:29.640 it. So anyway, the next day I had emergent brain surgery. And then being a physician in lung cancer,

01:18:40.520 you know, I was like, that can't possibly be, you know, I have never smoked. You know, how do I have

01:18:46.000 lung cancer? I am the healthiest person I know. I remember being in the hospital because of course,

01:18:50.680 you know, you're on drugs and everything else and shock and everything. And I kept saying,

01:18:55.260 look at my nails. These are the healthiest nails you've ever seen. How can this be a person who's

01:18:59.960 sick? Because somehow that was like just one example of how that's impossible. Talk about the stages of

01:19:06.980 grief and denial, right? And being a physician and knowing what lung cancer meant, the next thing that

01:19:13.600 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

01:19:18.480 know what this means for my family. And I don't want to play any part in this. I don't want them

01:19:22.640 suffering.

01:19:23.760 Can you tell folks what you mean by that? Not everybody might understand the implication of what

01:19:27.560 you're saying.

01:19:28.420 I wanted to go to Oregon because they had physician assisted suicide. Because I, you know, I knew I have

01:19:35.920 treated so many patients with lung cancer. I knew the horrible end. I knew what this meant.

01:19:42.720 But the suffering.

01:19:45.040 Especially when it spread.

01:19:47.020 Yeah. And it had spread everywhere. I mean, I had stage four lung cancer. You know, the day before

01:19:51.980 I had been fine, a hundred percent fine. That morning I had exercised vigorously.

01:19:59.780 And suddenly I'm in the hospital recovering from a brain surgery, being told that I have a rapidly fatal

01:20:09.020 disease. And, you know, all you can think of in that moment of panic is your family. Right. And so,

01:20:17.180 you know, my only thought was, I don't want them to watch me go. I want them to remember mom.

01:20:24.980 And so, I mean, there began my so far almost four year journey of a new me, you know, cancer changes you.

01:20:35.840 So, I'm not that person. One of the many things is sometimes at this point in time, you know,

01:20:43.440 I mourn that person. Because I really, I liked her.

01:20:50.860 I mean, one of the things that I think is very shocking for people to understand is that

01:20:57.700 probably between 12 to 14 percent of people who get lung cancer are not smokers.

01:21:03.360 And they all tend to get a certain type of lung cancer. You know, lung cancer is broadly divided

01:21:09.620 histologically by small cell and large cell or non-small cell, I'm sorry. And within the non-small

01:21:15.780 cell, there's large cell, adenocarcinoma, squamous cell. And most of the people like you who are not

01:21:21.000 smokers get this type of adenocarcinoma, non-small cell. And it is really shocking to think that

01:21:27.920 given the prevalence of lung cancer and the lethality of lung cancer, lung cancer kills more

01:21:33.820 people than any other cancer. And I believe that's true for male and female still.

01:21:38.900 Yes. I mean, by far.

01:21:40.780 Yeah. To think that such a high percentage, 12 to 14 percent could be non-smokers,

01:21:45.680 tells us the severity of this.

01:21:48.020 I also think it's worth reiterating something you've said, which is sort of the miracle of

01:21:53.440 the fact that we're sitting here having this discussion four years later. The median survival,

01:21:59.700 meaning if you took 100 people with stage four, which means a type of cancer that has spread from

01:22:07.340 its original site of origin, and in your case, it went to your brain, which is a particularly

01:22:11.260 devastating place for this cancer to grow. The median survival of people with stage four

01:22:16.740 lung cancer is probably 12 months or less, correct?

01:22:21.080 Well, it depends on what kind of lung cancer that you have, and sometimes even eight months or less.

01:22:28.900 Those were the stats that I knew when I was first diagnosed. And one of the things that I'll say is

01:22:37.960 non-smoking lung cancer is growing at scary rates. It's being diagnosed, and it hits people

01:22:47.020 in their prime. It's growing rapidly, especially in young women. So it's hitting a lot of moms. 0.98

01:22:55.320 Much more common in women than it is in men, although it does happen in men. Happens in Caucasian 1.00

01:23:02.180 and Asian women predominantly. And the interesting thing is most of the people that it impacts

01:23:07.760 are thin and in shape or athletes. So it goes against everything.

01:23:14.820 Do we have any insight into why?

01:23:18.320 No. And it's one of the things that's not being investigated as much. When you look at,

01:23:25.000 okay, what studies have been out there? Oh, we get the typical. It's radon. It's being next to a

01:23:30.740 smoker. I never was. Okay. My father was a smoker. He quit smoking the day I was born and never went

01:23:36.300 back. I was not raised around smoke. So the fact of who it's impacting and the fact that the demographics

01:23:47.140 of the people that it's impacting are the healthy people, unlike what we associate with our epidemic

01:23:56.280 of insulin resistance, that's not who these people are. We know that insulin resistance is responsible

01:24:02.220 for a huge number of cancers and cancer rises. That's not this. It's young women, and again, 0.96

01:24:11.620 who have presumably done everything right. And it's just, it's something that is not getting enough

01:24:18.640 press. I know the Guardian did a big story about it about a year ago, but otherwise it's not getting

01:24:25.300 the attention it deserves. And these women really wind up with two different kinds of cancer. They 1.00

01:24:32.060 wind up with EGFR-driven cancer, that's epidermal growth factor receptor, or they wind up with something

01:24:40.360 called ALK-positive cancer. I have the EGFR, specifically something called EGFR-exon 19 mutation.

01:24:52.060 And the thing I didn't know at diagnosis, because again, I had been focused on obesity and metabolic

01:24:59.120 disease and diabetes for so long, I hadn't been seeing as many people with active cancer as I did when I was

01:25:07.620 in primary care. And so I was quite frankly behind on some of the newer treatments and newer

01:25:17.140 diagnoses, if you will, and we're talking the genomics of cancer. But for EGFR cancer, there was

01:25:26.740 something called a targeted therapy. This class of medications is called tyrosine kinase inhibitors,

01:25:34.500 and people can go on them, and they can get better, okay? They can even, in many cases, have all of the

01:25:43.440 cancer go away. Doesn't mean they're cured, though, because it always comes back. And so after initially,

01:25:52.980 again, going through all these, I mean, I'll tell you, the denial grief stage.

01:25:58.360 I want to actually ask you exactly about that, Sarah. I want to go back to what is it like when

01:26:04.360 you were recovering in the hospital from the brain surgery? Because I assume they had not taken out

01:26:09.020 the primary tumors in your lungs. They were just alleviating the most life-threatening symptom you

01:26:14.780 had at the moment, which was a mass inside a part of your body that can't accommodate a mass,

01:26:19.500 which is why you had a seizure. So they take that out. You're recovering from a surgery that by itself

01:26:25.260 is difficult to recover from, but then coupled with the knowledge of, here's this disease, and

01:26:31.180 my lungs are full of this. What do you remember of those days?

01:26:37.840 Overwhelming grief to the point of not being able to think. You know, of course, I come and approach

01:26:44.020 everything in life as a mother. And I'm not saying as a mother only, like fathers would do the same

01:26:49.900 thing, but you approach every problem in life through what it means for your children.

01:26:57.940 How old were your children at the time, Sarah?

01:26:59.980 They were 7, 12, and 14. And they needed me. They still need me. And so the grief is overwhelming

01:27:12.020 about what I quickly realized is, I'm going to break my children's heart. And there's not a thing

01:27:21.200 I can do about it. And to have that realization, because it comes quick, and have to sit with that

01:27:29.800 is a grief I can't, I can't even explain. And so initially I just was, I couldn't handle the grief. I

01:27:45.680 had to be in denial, in denial. I came home from the hospital. I had just been discharged from ICU,

01:27:53.200 and I walked seven miles the day I got home. And my feeling was, see, I can't be sick.

01:28:01.040 I just got out of the brain surgery. I'm still on medication. I walked seven miles today.

01:28:06.660 I'm healthy. I don't know what you people are talking about.

01:28:09.820 What did your kids know at this time? Had your husband already spoken with them?

01:28:14.460 Well, sadly enough, and I actually didn't find this out until quite a bit later,

01:28:18.540 they are the ones who found me in the basement. So, you know, talk about not telling the children.

01:28:27.320 That was never an option for us. So they knew I was having surgery,

01:28:36.500 that there was a tumor in my brain, and that this was cancer. This is not good.

01:28:41.100 And that's a lot for a kid to unpack, right? Especially a kid, you know, again,

01:28:52.320 it's hard for any kid to unpack. But, you know, one of the things I remember when my kids were going

01:28:57.340 through each of their own, every kid goes through at the phase of, what if something happens to you,

01:29:03.120 mommy? What if something happens to you, daddy, right? All kids go through that. And the one thing

01:29:08.180 we used to kind of laugh together, my husband and I, about that. Say, oh, honey, your mommy and daddy

01:29:15.300 are the healthiest people. We are so healthy. You don't need to worry about that. And I remember that.

01:29:22.900 You know, it's one of the first things that you think of when you're put in this situation is,

01:29:27.380 oh, my God. You know, they have to unpack this in that context.

01:29:33.440 And it's hard to be a teen. It's hard to be a seven-year-old.

01:29:40.580 But to be one whose mother suddenly had a,

01:29:44.000 you know, diagnosis of advanced cancer.

01:29:48.720 And we, it was a hard decision on what to do, but,

01:29:53.940 you know, in talking and how do we handle the kids. But the one thing we decided together,

01:29:57.780 I mean, my husband and I, is that we were never going to lie to them.

01:30:03.640 We were always going to tell them the truth because I thought that the worst thing for a kid

01:30:07.780 is to constantly be wondering if something, if there's going to be a huge shoe that drops.

01:30:13.840 And so we told them, we tried to open up the lines of communication. They

01:30:19.240 mostly didn't want to talk about it,

01:30:22.460 but we told them that we were making that promise to them. And we have never,

01:30:27.400 never gone back on that problem and promise and never will.

01:30:31.220 I mean, that's one that it's really important to me.

01:30:34.100 We may delay telling them something for a little bit until we really know the facts.

01:30:39.780 But as soon as we really know the facts, they're going to hear about it.

01:30:43.760 And over time, in grief, you learn to accept many things.

01:30:52.480 My husband and I, our dream had been to retire to a farm and make gourmet butter.

01:31:00.520 Like, that's what we were going to do. That was going to be the second career, right?

01:31:04.320 And you learn to make peace with that's not the case anymore.

01:31:08.020 You know, our, we always used to joke that the way we wanted to die was 95 years old on the way

01:31:16.240 home from a skiing trip in a fiery car accident where our kids would not have to deal with the

01:31:22.840 bodies, but we wanted to make sure it was on the way home.

01:31:26.240 The cremation, the two for one.

01:31:28.620 A two for, it was going to be on the way home because we were going to be having fun up until

01:31:34.140 that point. So that's acceptance. You know, you're not going to retire. You're not going to

01:31:39.260 have all these things, but you can't accept that you're not going to be a mom. Impossible.

01:31:47.940 Now, at some point, I'm guessing kind of the problem solver in you started saying like,

01:31:54.300 Hey, I'm going to learn as much as can be known about this. And we're going to talk about this in

01:32:00.640 the context of the asymmetry that exists. I just had a discussion about this with,

01:32:06.300 we have a weekly meeting in our practice with all the providers. And, you know, we just had this

01:32:12.140 weird situation recently where, you know, basically a patient of ours who has another physician

01:32:18.780 was kind of caught in the middle of a recommendation that turned out not to be the

01:32:23.400 right recommendation. And, you know, we were able to get them a referral to somebody else who

01:32:28.060 basically got them out of a very unnecessary surgery. And we were just sort of thinking,

01:32:34.440 man, like, we're so glad that that patient was able to dodge that bullet. You know, they were going to

01:32:38.520 have a surgery that they totally didn't need. That's a very big surgery with lots of risks.

01:32:45.600 And we realized like the asymmetry of knowledge in medicine is so overwhelming that it is,

01:32:53.440 it's not even just about money or education outside of medicine. Like a smart person still

01:33:00.900 has a hard time digesting medical literature. And like I said, we're going to talk about this,

01:33:05.760 but, you know, you very quickly must've figured out, Hey, I have this EGFR-19 deletion.

01:33:12.860 So we no longer talk about this as you have lung cancer or you have adeno or you have non-small

01:33:19.280 cell. We're really going to refer to it by its mutation and everything will come down to how do

01:33:23.420 we treat that? How long was that process for you to say, I'm going to, I don't know if this is the

01:33:30.640 right word, but I'm going to partition my grief and my problem solving brains and I'll do both of them,

01:33:37.340 but I'll, I'll move back and forth. It happened pretty quick, which is, okay,

01:33:43.480 this is terminal, right? You have to come to grasp at that, but terminal when and what can I do to

01:33:53.360 control the when? But when you say that, Sarah, did you really come to that realization so soon?

01:33:59.440 Because technically life is terminal. I mean, there's nobody listening to this podcast,

01:34:04.740 watching this video who isn't going to die. So that's all terminal. But when you say that,

01:34:10.600 do you mean that immediately and without question or reservation, you felt that you would not live

01:34:17.700 a normal life expectancy? There was no hail Mary out there that was going to take you to being the

01:34:23.580 95 year old skier. Yeah. I mean, I, I think just the reading and understanding, although the advances

01:34:30.700 that this was going to be terminal really soon, you know, in my life. And I was only 46 at the time.

01:34:39.800 And, you know, my first thing was just, please let me make it to 50. I'm 49.

01:34:47.440 You're going to be 50 soon. Yeah. I'm going to be 50 in the not too distant future. So, you know,

01:34:53.240 that was like, my first one was just like, okay, let's, but right from the beginning, I'll tell you

01:34:59.160 the when was 11 years. Okay. And that has not left. I don't need to be 95. I can accept all those

01:35:08.640 things that I'm going to miss out on by not growing old. I just need 11 years, which to everyone was

01:35:16.620 unrealistic, but why 11 years? Because my youngest would be graduated. So immediately my goal was,

01:35:27.880 I can't settle for less than 11 years. I have to make it to 11 years. And so in became that,

01:35:36.140 like my war cry, 11 years, 11 years, I have to make it 11 years. And that started me on a path of,

01:35:43.860 oh my gosh, so much. So the first thing I thought in reading all the, I mean, read everything is,

01:35:49.760 I got to get this primary tumor out. You know, I'm considered inoperable, but we know that having

01:35:55.880 this primary tumor here increases my risk for mutations. Okay. Remember I said that the tyrosine

01:36:01.620 kinase inhibitors or the TKIs, they work amazingly well, but only so long, you know, somewhere between

01:36:10.240 eight and say, you know, on average eight and with the more advanced ones at the long end is like 24

01:36:20.320 to 30 months. Okay. So that's not enough time. That doesn't get me to 11. So I was like, okay,

01:36:28.820 you know, this is increasing the risk for mutation, which is how these develop resistance to the

01:36:34.320 tyrosine kinase inhibitors. And remind me, Sarah, you, because I remember you emailing me probably

01:36:40.760 by August and starting to explain some of the details. Your biggest tumor was like five centimeters.

01:36:48.560 That's a monster tumor. How many tumors did you have? It was six centimeters or you had six tumors?

01:36:54.600 It was six centimeters, which is amazing in the sense that I never had pain from it.

01:37:00.560 I never had a cough. Probably because you were so healthy.

01:37:05.240 I think so. Because talk about being caught out of the blue, you know, there just wasn't this

01:37:09.600 premonition of something is awry and I'm just not addressing it.

01:37:13.740 So the standard of care was just that we typically don't operate on patients with metastatic tumors.

01:37:20.520 It's, it doesn't, the only reason they operated on your brain was it was an acute way to save your

01:37:25.440 life. I think it's hard for patients listening to this to understand that, but that's the play.

01:37:30.460 We look in oncology, right? When a patient shows up with metastatic cancer, they're considered not

01:37:35.900 surgical candidates. And this was the exception and not the rule. You were going to be dead probably 0.84

01:37:41.300 within days if they didn't operate on your brain. But all this time afterwards, you still have these,

01:37:47.800 this burden of tumors in your lung. And now the question is, can we improve your prognosis?

01:37:54.140 And maybe that doesn't mean you live to 95, but can we reduce, can we make your cancer less

01:38:01.260 resistant to therapy by taking the majority of the cancer cells out of your body?

01:38:06.820 Right. And decreasing the tumor burden because really quickly the TKI got rid of every single

01:38:13.720 small tumor. I had them throughout, you know, like paint splatters on throughout both lungs.

01:38:19.720 And they were gone in a matter of weeks. That's staggering, isn't it?

01:38:24.560 I mean, it is. It's, it's remarkable, but you know, again, the primary tumor was huge. So I had,

01:38:31.820 unfortunately, the large tumor in my brain was not the only one. I had two other ones that they

01:38:37.520 radiated. They didn't need to be surgically removed. They were small. They could be radiated.

01:38:42.100 And then I set about trying to find someone who would take out this primary tumor.

01:38:48.300 Can I ask you about the stereotactic radiation, Sarah? That's, I mean, we glossed over that,

01:38:52.940 but that's not a benign process either. Did you suffer nausea from that? What,

01:38:57.720 how difficult was your stereotactic treatment? Did you take it all in stride?

01:39:02.440 I did great with the treatment to the brain. I didn't have any issues. You know, I did have issues

01:39:10.060 at the beginning, but they were more to the TKI. You know, one of the things with every specialist

01:39:15.400 that I saw, they couldn't believe it. Or they told me if I saw them earlier, it wasn't going to happen.

01:39:21.860 You know, at least you'll keep your hair. All my hair fell out. Like it wasn't supposed to happen.

01:39:26.760 Like your hair is not supposed to fall out with TKIs. All my hair fell out.

01:39:31.640 Anyway, so the brain radiation went fine. And then I met a surgeon who was going to

01:39:37.300 take out the primary tumor for the reasons that I was saying. We just, anything to decrease the risk

01:39:44.040 of developing a mutation that keeps me from being sensitive to the TKIs. And so I went in

01:39:52.440 for surgery in September and I can remember her saying, we're going to take this tumor out. We're

01:39:59.920 going to take out your right upper lobe. Unless of course, we've seen that there's disease in the

01:40:05.600 mediastinum. But there was no disease on the PET scan in the mediastinum. So she was feeling pretty

01:40:11.840 positive about being able to take that out. But I knew for several weeks beforehand that that was

01:40:19.600 a possibility. And just so folks know what we're saying, on the right-hand side, you've got these

01:40:25.080 three lobes here, but they drain into these lymph nodes that are in this middle structure called the

01:40:33.320 mediastinum. And so you had this monster tumor that was going to require the entire upper right

01:40:39.600 lobe to be taken out. But if the surgeon felt that on visual inspection, at least, or maybe even

01:40:46.480 sampling nodes that any of those nodes had cancer, it was her opinion that this is really futile because

01:40:53.160 now we know it's already escaped the lung. It doesn't matter. So you went into that surgery

01:40:58.440 knowing you could wake up with a huge scar in your chest, chest tubes coming out and the cancer is

01:41:05.740 still in you, right? And that happened. And that was, it was terrible. I kept apparently under the

01:41:14.160 influence. I mean, everyone told me I was so hysterical screaming in the recovery room. I'm a

01:41:22.080 mom. You can't let this happen to me. I'm a mom. That's all I kept saying. And I of course don't

01:41:26.580 remember any of this, but they had to actually take me away, put me in a private room. And that

01:41:31.980 was all that I kept saying. So, you know, I had to come home and learn to accept that. I now was bald

01:41:40.720 and I definitely fell into a deep depression, but at the same time I refused to completely give up.

01:41:52.600 I mean, like, for example, I went back to work at the clinic the same month that I had brain surgery,

01:41:56.580 which sounds crazy, but it's just part of this whole process. And then, but after the surgery

01:42:05.140 failure, that was terrible. And then I didn't really recover back into my determined place until

01:42:13.920 a really very specific moment. And that was just a couple of weeks before my diagnosis. I had been

01:42:23.420 selected to be an Aspen Health Innovator Fellow, which was, I mean, this is among the highest honors

01:42:29.580 for your work. The Aspen Institute is a place that brings together thinkers in all kinds of disciplines

01:42:37.460 disciplines. And to be chosen to represent people who are innovating in the healthcare space was

01:42:43.020 such an honor. And in order to do that, you had to commit to four weeks of leadership sessions

01:42:52.180 in the next two years, which of course, at the time I was like, of course, sign me up.

01:42:57.660 But as that first session inched closer, it was in November, I was so, what do I do? I couldn't make

01:43:06.620 up my mind. I literally didn't make up my mind for sure until I sat, I got on the airplane

01:43:12.600 because I was ready to run back because it was like, I'm going to leave my kids

01:43:18.660 for almost a week. I have terminal cancer. And at that point I decided you can live feeling sorry

01:43:27.980 for yourself and of all the things that you're going to lose, or you can go out and live and

01:43:36.300 your kids are going to be better for it. This is what really made me decide your kids are going to

01:43:41.020 be better if you choose to live. And so that was the moment sitting on that plane seat, crying,

01:43:48.040 never, I've cried on a lot of planes since this diagnosis, deciding I just chose to live. This

01:43:55.800 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

01:44:02.420 since then. Because I have a platform. I had a platform. I had done what I feel was a lot of good

01:44:13.620 for a lot of people and it wasn't finished. And I knew that this was good for my children. And I'll tell

01:44:21.900 you one of the most impactful moments of my whole life happened before my diagnosis. And it was one of

01:44:30.860 these times where we were at the dinner table and the lottery happened to be one of those, you know,

01:44:37.300 hyperinflated lotteries. Oh my God, you can win, you know, bajillion dollars. And so my husband and I

01:44:43.340 were at the dinner table joking around about it, right? I mean, we don't play the lottery, but we

01:44:48.200 were joking around. Maybe we should buy tickets, you know? We could retire. We could retire. And here at

01:44:53.300 the time was my 13-year-old son at the dinner table. And he got really upset about us discussing this.

01:45:00.960 You can't retire, mom. You're doing so much good for the world. How could you even think of it?

01:45:09.540 I've never been so... That is a defining moment in my life. And like, I was like, oh my God.

01:45:19.760 You know, at the time I just, I was so taken aback by that. Certainly that weighed heavily on my

01:45:26.740 decision to get on that plane and to continue doing what I'm doing. And what I'm doing has morphed

01:45:34.740 since my cancer diagnosis into an even greater focus on health equity because of my experience

01:45:42.560 as a cancer patient and someone who is privileged. Because I'll tell you, you have a much greater

01:45:52.760 chance of surviving cancer if you are, uh, has privilege, you know, one of the lucky ones.

01:46:03.980 And I didn't realize the stark differences until I became a patient.

01:46:12.520 I want to talk about that in some detail, Sarah, but I want to also understand

01:46:17.680 how it is that we're still talking today, frankly. In other words, how have you managed to

01:46:26.540 stay in an equilibrium with this disease, right? I've always, I mean, let me, let me share with you

01:46:33.600 a couple of things that I, I've always struggled with when thinking about cancer. I, I'm not fond of

01:46:39.660 the language that we sometimes use around cancer and that we beat cancer and that we can't give up

01:46:47.740 and things like that because it almost suggests that the patients who don't survive cancer have

01:46:52.200 somehow given up. And I, I just, I, I just don't find that in my experience, having taken care of

01:46:57.500 many patients with cancer to be true. I think, you know, it doesn't make sense to me. And I think the

01:47:02.600 way that you said it and described it earlier makes the most sense, which is basically finding a way to

01:47:08.520 coexist with your cancer for as long as possible. And you've exceeded all odds. I want to kind of

01:47:16.300 understand that journey a little bit more. It's one thing to go through the tyrosine kinase inhibitor,

01:47:22.280 have this immediate response that's remarkable, but then get this setback three months later where

01:47:29.200 your primary is not only still there, but you actually realize now there's, there's mediastinal

01:47:33.620 involvement, which basically means there's no question you have cancer cells elsewhere in your

01:47:39.020 body. It's not like they stop when they get to the lymph nodes. So pick the story up for us in terms

01:47:46.200 of what your ongoing treatment has been life. Like how have you stayed in this, in this state of

01:47:51.920 equilibrium, so to speak? So I haven't. Okay. On many occasions, I haven't. So after the surgery,

01:48:01.300 the next thing that happened is they found another brain tumor. There's argument as to whether it was

01:48:07.760 there from the get-go or whether it was something new, but either way they decided it would be considered

01:48:16.600 that the first line TKI that they had put me on had failed me. And so I got switched to, I got more

01:48:26.500 radiation to the brain and I was switched to the newest TKI, happens to be called osmertinib or

01:48:35.220 chagriso. I was put on that in November, right before I went off for my first Aspen Leadership Conference.

01:48:44.280 And I had decided that I do not accept being a sitting duck because what the cancer world then

01:48:57.440 wants is for a patient like me to just sit and wait for the cancer to come back, right? That's

01:49:05.820 what you're doing. You know, it's coming back. There's no question about it. And you know,

01:49:09.480 it's coming back soon. And you are just waiting. And I couldn't accept that as a mother. I think I

01:49:18.700 could accept it as a human, but I couldn't accept it as a mother. And so I went on a journey to find

01:49:27.020 someone who could treat me in the most aggressive way possible, who shared my view that sitting around

01:49:37.700 and waiting for this to come back was totally unacceptable. I traveled the country. I saw

01:49:45.560 everybody. Let me tell you. First of all, of course, that shows I have means to do that, right? That a lot

01:49:50.920 of other people don't. And I actually, along the way, met another mother, physician, my age, just a bit

01:50:01.080 younger, younger kids, who had the same attitude towards it. I refused to accept this. We sort of

01:50:08.660 became a team, so to speak, and wound up by complete serendipity, meeting a group of physicians

01:50:17.440 who really felt that the way to treat this long term was to be constantly battling it with something new.

01:50:28.860 So in other words, the cancer dogma right now is you put people on something at the highest dose

01:50:35.440 possible, and you keep going until it doesn't work anymore. That's how we deal with cancer. And then

01:50:43.060 we switch, and it's the same thing over again. And the idea is, what if we hit it with less and then

01:50:51.280 change it up all the time, right? And this goes to the idea of beating the mutations before they can

01:50:57.940 get you. So thankfully, I had a physician here at home who was willing to say, okay, that is worth a

01:51:09.560 shot. February 2019, okay, because it took a long time to get to this point, right, of searching, trying

01:51:17.780 to find something. I started chemo, regular chemo. I went through the regular cycles of chemo.

01:51:26.460 And then when I was done with that, I immediately went to anti-estrogen therapy, okay, because I had

01:51:35.020 a very specific mutation besides the EGFR1, and there was a medication to treat it. It just so happened to

01:51:44.560 be a breast cancer medication, but it was the same mutation for either cancer. So immediately upon

01:51:53.140 stopping the chemo, I went on the anti-estrogen therapy. So I was put into early menopause with a

01:52:02.820 number of regular medications, Lupron, Fulvostrant, and then I was started on a medication called

01:52:09.420 Pablacyclib, okay, which again is primarily a breast cancer medication, but was targeting one

01:52:15.780 of my very specific secondary mutations. I was on that for the summer, and all this time, I'm still

01:52:22.140 on the Tigriso or Asimertinib. That never stopped. As soon as the eight weeks of that was over with,

01:52:28.520 I went back on chemo, but very different. Low dose chemo. Single agent, very low dose.

01:52:38.500 So the first one was Cisplatin. And, you know, everyone says, oh, Cisplatin, you know, you're

01:52:44.480 going to do terrible on this. I mean, this is harsh, and it is. But, you know, I did fine. I mean,

01:52:50.860 I'm not saying I wasn't tired. I've basically been nauseous for the last almost four years,

01:52:57.140 every single day. You know, it's just you learn to manage that. So I learned to manage it. I learned

01:53:02.380 to manage, you know, being tired and the things that came along. I still traveled for work. I was

01:53:08.240 still able to do everything. I just, I could tell you some really crazy stories of things I had to do

01:53:15.040 while traveling to accommodate how I was feeling that nobody knew about at the time. But anyway,

01:53:22.440 some really wacky stuff that you do, but you just, you manage, you figure it out, right? You,

01:53:27.140 you improvise, lots of improvising. And then I got switched to another, after eight weeks,

01:53:33.900 got switched to gemcitabine or gems are. Which again, these are so crazy. You just don't think

01:53:40.140 of this because that's a drug that's typically used in pancreatic cancer, right?

01:53:44.480 Well, yeah. And it can be used in lung cancer too.

01:53:47.300 I mean, it just depends on the mutation. I think that's the point, right?

01:53:50.100 Right. Yeah. Believe it or not, there's no standard chemo for lung cancer.

01:53:53.680 Can you believe that? There's not a standard, like standard of care regimen. So the thing is,

01:53:59.400 I wasn't doing any outlandish things here. Okay. These are all treatments for lung cancer.

01:54:05.680 Like you said, gems are, is used more for other things, but this is not an outlandish thing that's

01:54:12.020 never heard of for lung cancer. I mean, same with cisplatin. I mean, none of these things are,

01:54:17.420 or, you know, I was, oh my goodness, we're going to, you know, do something, you know,

01:54:21.580 that's never, ever been done before, you know, so to speak things.

01:54:24.800 And at this point, which is now the fall of 2019, where, if you go and get a PET scan,

01:54:32.900 where do you actually have tumor in your body at this point?

01:54:35.460 So yeah, let me back up for a second because, well, the quick answer is I had no tumor. There

01:54:42.640 was no tumor anywhere. And to back up is that the Tigriso, this is pre-chemo, had stopped shrinking

01:54:52.800 my primary tumor in March of 2018. So this was, you know, almost a year before I began chemo.

01:55:03.740 And so since they wouldn't surgically operated to get it out, I had it radiated. Again, I was lucky

01:55:12.700 enough to have a radiation oncologist who worked with me. And like I said, I tolerated brain chemo

01:55:20.040 well. The same was not the case to the lung. I had real issues. And interestingly enough, we were

01:55:30.800 leaving for, to hike the Inca Trail in May of that year. So I had had radiation that we're leaving

01:55:39.040 to hike the Inca Trail. And I started having kind of bad chest pain, like a day or two before we

01:55:44.440 hiked the Inca Trail. I was like, okay, I'm sure this is just reflux. I'm going to take some reflux

01:55:49.500 medication. And then I was like, look, okay, if it's not, if it's more, you know, what a better place

01:55:55.440 to die than surrounded by your family on the Inca Trail and all the beauties of the Andes Mountains.

01:56:01.520 Okay, I can accept this. Let's go. You know, I didn't even tell anyone. I was like going forward

01:56:06.380 and did that successfully. It was great. My eight-year-old toodling along, you know,

01:56:12.580 she was always the fastest of any of us. We went with our friends and I mean, amazing experience.

01:56:19.020 I just have to say that those things, especially if you can get kids in it, I'll never forget that

01:56:23.960 when we all got back and we went and checked into the JW because we were like, give me a shower,

01:56:30.540 a very clean bed and a spa. My middle child, my daughter said to all of the adults,

01:56:38.860 I developed my third eye during that. It was one of those experiences. Like you don't normally think

01:56:46.200 you're going to get that out of a, you know, she was what, 14 at the time. We were all like, what?

01:56:54.260 But anyway, so it was a super special time. I was still having pain. And then my rest of my family

01:57:00.300 flew home. I actually had to fly from Lisbon to Switzerland because I had a conference I had to go to.

01:57:08.240 And at that conference, things started to get really bad. I made it through, but not with,

01:57:15.100 again, some funny stories of how I accommodated to it because I was having crushing pain.

01:57:22.860 Got home. Turns out, of course, I had some rare, I had this rare complication where it actually

01:57:27.680 impacted my bones. My radiation oncologist said, the only treatment for this is to put you on long-term

01:57:34.780 opioid therapy. And I was like, oh, no thanks. I will accommodate. There was no way I was doing that.

01:57:41.420 So I had to get through that, which was a, which that was a little bit of a saga. But anyway,

01:57:48.680 I had no disease then after that radiation, none. And so I was in this state, they call it

01:57:54.760 NED, no evidence of disease. I like to always say NED, right? I was NED for a really long time. I had no

01:58:02.060 evidence of disease. It was a great place to be, right? Still on treatment, still trying to do

01:58:06.680 everything to keep this from coming back and started GEMSAR. And, you know, everybody had said

01:58:12.680 all these terrible things about cisplatin and GEMSAR was 10 times worse. Everyone was like,

01:58:18.460 you'll be a breeze. GEMSAR is a breeze compared to cisplatin. 1.00

01:58:22.520 You are really the exact opposite of everybody because, yeah, I mean, we used to tell patients

01:58:27.120 GEMSAR is, it's non-chemo.

01:58:29.580 Yeah. Everybody tolerates GEMSAR. I can still remember sitting because I was feeling too crappy

01:58:35.360 to drive, my mother driving to pick me up to take me to chemo one day, sitting on my front porch and

01:58:41.280 throwing up in a plant on the way to chemo. There are nutrients in there, Sarah, that are very good

01:58:46.480 for the plant. So I wouldn't feel bad about that. That's very, it's a very healthy part of the carbon

01:58:51.160 cycle, I'm sure. But I was determined to keep on. I was really close to getting switched to taxols,

01:58:57.260 which, you know, I'm like, this is going to happen, that'll be better.

01:59:01.000 So then had to take another trip for another meeting and had lots of friends there. And I can

01:59:09.980 remember them standing behind me after we had eaten and they were pushing me up this hill in San

01:59:17.400 Francisco because I literally couldn't walk. And I kept thinking to myself, I'm a hypochondriac.

01:59:23.280 This is just because I'm anemic, whatever. I was super short of breath, but I'm like, okay.

01:59:30.940 I had convinced myself I was making it all up in my mind. I fly back from that trip and the very next

01:59:37.260 morning head in for chemo. And they immediately said, oh my God, no chemo. Everything is a mess.

01:59:45.800 My liver numbers were through the roof. My kidney numbers were high. I had pancytopenia so bad.

01:59:53.440 How anemic were you, Sarah?

01:59:55.560 I was like six at this point. I mean, it was bad, really bad. The low sixes at this point.

02:00:01.560 Right. And just so the listener understands, the normal would be 13 or 14 of a hemoglobin and you're

02:00:06.960 six. So that's really low. And your platelets were how low?

02:00:10.720 23.

02:00:11.600 Which means you basically don't have the ability to form a single clot.

02:00:14.980 Right. I was a disaster. And the funny thing is I was still up and doing okay. You know what I mean?

02:00:22.760 I was tired. I was shortness of breath with activity, but I was doing okay. And they sent me home.

02:00:28.060 And I was like, that doesn't seem right. Am I crazy that I shouldn't be home?

02:00:36.120 So of course, I call some of my other physician friends. Aha. Privilege. Right. Because I was

02:00:44.180 getting sent home. And they're like, oh my God, we're admitting you right now. So I actually get

02:00:50.700 a backdoor admission to the hospital and a complete workup starting right then. I had to have a

02:00:57.180 thoracentesis, drained a whole bunch from my lungs. That was unknown when I got sent home.

02:01:02.660 So you had tons of fluid around your lungs.

02:01:05.600 Tons of fluid around my lungs.

02:01:07.360 That's explaining the shortness of breath.

02:01:09.040 Yeah. And once I was admitted, I was promptly transferred to ICU. Things were going downhill.

02:01:15.440 I had to be put on BiPAP. So I had multi-organ failure.

02:01:18.700 Had respiratory failure, liver failure, kidney failure. I was a big failure. Okay. Everything

02:01:24.880 was bad. And was this believed to be the result of your body's response to the tumor or the chemo?

02:01:32.380 It was the GEMSAR. So I got taken care of in the hospital. I just want to cry to think about the

02:01:41.000 care I got. It was so wonderful. And I just had the best team. I would have died. Nobody can

02:01:48.620 believe that this was well over a year ago now. And I'm healthy with no persistent failures because I was

02:01:59.960 near death. And I was in the ICU for a really long time. And everyone, every day, it went from,

02:02:07.620 I think your kidneys will rebound to 50-50. They're never going to be normal.

02:02:17.520 I was on plasmapheresis. And it turns out I had something called atypical hemolytic uremic syndrome.

02:02:22.720 And to just explain, over 70% of people are either dead or on dialysis, you know, right away. I mean,

02:02:31.440 it's got an incredible mortality, right? Incredible. It's incredibly difficult to treat.

02:02:39.740 And so, you know, outcomes are you're dead or you're on permanent dialysis. So I was put on a new

02:02:48.560 medication after, you know, going through kidney biopsies, all these kinds of things in the

02:02:53.320 hospital. Sent home, did outpatient plasmapheresis for a while. And then things miraculously started

02:03:01.700 getting better, right? Not miraculously. It was because of this medication I was put on.

02:03:06.060 Of course, that meant an infusion every eight weeks. And the worst part to me is it meant no one would put

02:03:11.160 me back on chemo. Just they wouldn't put you on GEMSAR or they wouldn't put you on anything?

02:03:15.400 It wouldn't put me on anything. And to me, that was devastating because I said,

02:03:21.140 well, kidney failure is one thing, but having this cancer that we know come back is another.

02:03:27.180 So that was another hard pill to swallow. And long story short, I got better. I went to

02:03:35.280 pharmacogenetics, which is where they actually take a look at what your genetic profile is in response to

02:03:42.340 different drugs. And it turns out I had a genetic mutation. Hey, I have lots of them.

02:03:50.080 It turns out I had a genetic mutation that didn't allow the GEMSAR to break down. So I was getting

02:03:56.320 toxic doses of this. And I was on a very low dose. But the thing is that I couldn't get rid of it.

02:04:03.980 So normally, if you see atypical hemolytic uremic syndrome with GEMSAR, it's after months and months

02:04:09.640 of treatment. And I got this within four weeks. Why? Because I was getting mega doses of it because

02:04:18.420 my body couldn't get rid of it due to this mutation was the explanation. You know, and they

02:04:24.100 said, there's no reason you can't take any other chemo. This is very specific to GEMSAR.

02:04:28.840 But that was that. Sit and wait mode. Back to sit and wait mode. And it took another year,

02:04:39.980 but the cancer came back in September of 2020.

02:04:44.540 And here's my story from that, which really made me so determined to work even harder for health

02:04:57.660 equity. Here I am, a physician, able to grasp really difficult concepts, able to read and scour

02:05:07.540 the literature and know what I'm looking for, able to call at a moment time, you know, anytime someone

02:05:13.920 to help me sort through something I didn't understand, or help maybe refer me to someone.

02:05:21.540 You know, I had all the resources in the world. And the reoccurrence was in September.

02:05:29.680 Even with all my constant pushing and self-advocacy, the one thing is I had, by the time I was diagnosed

02:05:39.740 with cancer, I was an expert patient advocate. Expert. Hardcore. And, you know, one of the other

02:05:48.680 advantages I had is it didn't take much to switch that and to become a self-advocate, an advocate for

02:05:53.860 myself. So I was diagnosed in mid-September with a reoccurrence. I did not get on a clinical trial

02:06:03.640 until I got started December 30th. That's a four-month delay. That's a four-month delay for me.

02:06:15.060 And in hindsight, now, looking back, before I was panicked, right? And I couldn't really,

02:06:23.900 I was like, something has to get done. Something has to get done. Something has to get done.

02:06:29.140 I can look back in hindsight and say, how many people die during that time?

02:06:36.500 How many people who don't have the advantages I had just die during that delay?

02:06:46.600 How many? I shudder and I just want to cry. And what I've done is I've reached out to other cancer

02:06:55.080 patients to say, has anyone else been in this situation? And I find out it happens all of the

02:07:03.900 time. It seems that we have a really good system. As I experienced, when someone is diagnosed with

02:07:11.020 cancer, they get a health, a cancer navigator, you know, they get all these things and we're

02:07:17.100 boom, boom, boom, boom, boom. But when that cancer comes back, it's kind of like the system seems to give

02:07:21.600 up on you. I had to advocate the heck out of getting a biopsy done. A biopsy that would be enough

02:07:32.100 tissue to make me eligible for a clinical trial that would actually get me a full genomics report.

02:07:40.500 I mean, that wasn't going to happen. I'm telling you, I had to get almost obnoxious about it.

02:07:46.880 And the stories that I'm getting from people are the same.

02:07:51.260 Where was the recurrence?

02:07:52.660 In my right upper lobe.

02:07:55.060 So they had to get, you had to get another lung biopsy to do this. And can I ask you another

02:08:00.840 thing, Sarah, what has been, you obviously have health insurance, but I assume that there's been

02:08:06.320 a non-trivial amount of out-of-pocket costs as well in the last four years?

02:08:11.260 Oh yeah. Oh yeah.

02:08:13.160 Do you have a sense of what the out-of-pocket cost has been for your care?

02:08:18.040 Tens of thousands of dollars.

02:08:19.360 Which obviously speaks to another challenge. I don't know if this is still true, but

02:08:24.420 it certainly was true at one point that the greatest source of personal bankruptcy in the

02:08:30.720 United States is healthcare and inability to pay healthcare costs.

02:08:35.400 And a cancer diagnosis is so high up there.

02:08:39.460 I would have to believe that cancer is the leading subset of that as well.

02:08:44.780 And so now I'm like, especially when I got feedback that I'm not alone in this, it wasn't

02:08:54.440 just me, you know? And again, I always keep saying in the backdrop of I am one of the privileged

02:09:01.440 and I was put in this situation. And the fact of the matter is by the time the reoccurrence

02:09:06.920 was diagnosed to the time I finally got treated, I had progressed so much that I had compression

02:09:16.520 of my bronchus. I couldn't get up a flight of stairs without desaturating. I mean, this all just

02:09:21.300 happened. I was in horrible shape, which of course, again, and remember, I'm starting out

02:09:28.960 before my diagnosis in general, I was so healthy, which gives me an advantage in this, which gives

02:09:37.580 me a significant advantage in this. But it goes back to that question of how many people just die?

02:09:44.280 Sarah, you're very realistic about the fact that your time on this earth is less than it should be,

02:09:53.020 right? A 49 year old, otherwise healthy person who's done all the, you know, done the right

02:10:01.060 things for their health should have another 40 years on this planet. And at least statistically

02:10:06.160 speaking, that's, that's not, doesn't seem likely. It suggests to me that you're very cognizant of how

02:10:13.200 you spend your time. So should take a moment to thank you for spending a couple hours with me here.

02:10:19.840 But how do you now think about the time that you allocate to your family,

02:10:28.460 to your work in the diabetes community, and now to this third important pillar to you,

02:10:36.680 which is cancer advocacy? How are you managing that? And how do you, how do you think about

02:10:42.140 how to even balance that? Because I think time is the most important currency. I think everybody

02:10:48.020 can appreciate that in a vague sense. It is the great equalizer, but of course, most of us can't

02:10:56.500 appreciate it the way you can, because you have a real visceral appreciation for it that comes

02:11:02.440 exactly with this type of an illness. And so therefore, I think that your appreciation for

02:11:10.020 the balancing act of what you described earlier, which is living your life to the fullest,

02:11:16.520 regardless of its duration, that's your legacy. That's what your kids are going to remember about

02:11:22.560 their mom, being the advocate for other patients, so that in 10 years, when another Sarah Halberg gets

02:11:30.140 this diagnosis, even if she doesn't have your education or your means, she can have an extension

02:11:36.800 of life the way you do. It's a bit overwhelming for me to think about how I would do that. Because

02:11:41.480 as I put myself in your shoes, my intuition is I'd want to retreat from everything outside of life,

02:11:47.640 everything outside of my family. Like I would imagine, and it's hard to put yourself in another

02:11:52.940 person's shoes without being there. But my intuition is I would say, I don't care about anything outside

02:11:57.240 of the walls of this house. And I would take a selfish approach in some ways, I think. And you've

02:12:03.820 done this very selfless thing, which is continuing to sort of prioritize everything else as well.

02:12:10.140 How do you do that?

02:12:12.080 A couple of things. Number one, believe it or not, originally, it was actually hard to be around my

02:12:18.180 kids when I was so deep in grief because, and that sounds crazy, right? That sounds counterintuitive,

02:12:26.140 but they reminded me of everything I was going to lose, right? They were what I didn't want to lose.

02:12:32.400 And so it was challenging. And I knew I had to overcome that. That was a big motivator for me to not be

02:12:39.840 thinking about that and thinking in that way. And I'm happy to say I clearly have overcome that, but

02:12:47.440 my kids come first. You know, I'll drop anything and everything if they need me now. But I also think,

02:12:54.740 again, and I go back to sort of what I alluded to before, they need to see me not getting knocked out

02:13:02.500 by the stressors and bad things in life. You know, I mean, bad things happen to good people.

02:13:10.980 Like I said, there's been a pivot in every part of my career based on anger. And I certainly am angry

02:13:16.920 about this. But what do you do with it? That's what's going to be the important question in life.

02:13:22.380 You can take anger, you can take all these things, and you can get lost and buried in it. Or you can

02:13:28.600 try to turn it into something else. And I have to say, I haven't become as big a cancer advocate yet,

02:13:37.340 and I'm working on it. But the reason for that is, and this was a question I had to ask myself a long

02:13:44.380 time ago, which is, shouldn't you be a cancer advocate now? But I have a platform for diabetes.

02:13:50.660 And damn it, that's important too. All these people suffering from this is important. 0.96

02:13:56.320 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.

02:14:03.140 It doesn't mean I'm ignoring it. But it's like, it makes me want to work more again for health equity,

02:14:11.000 because it spans both, right? It has to do with both diabetes and cancer. And that is so

02:14:20.220 important. So yeah, how I spend my time is really critical. And I want to say, it's not like I'm,

02:14:28.940 I don't want to paint the picture that, oh my gosh, I'm the superwoman. I have a terminal cancer. And

02:14:34.920 yay, life is great. No. When people ask how I'm doing, okay. If I say okay, you know I'm doing okay.

02:14:46.020 There's never good or never great. Okay. And that's just where I live right now. I'm definitely

02:14:52.940 not sitting around and feeling sorry for myself. Okay. Definitely not, not enjoying things in life.

02:15:01.300 But great is hard to think about. You know, great is hard to think about now. And some people say,

02:15:08.660 well, so cancer really helped me get a new perspective on life and what I care about.

02:15:14.260 And I'm happy to say, I don't know that I got that. Okay. I mean, having cancer sucks. And I'm

02:15:22.300 still mad about it. And you know, sometimes I have to sit and have a pity party every once in a while,

02:15:28.140 because the fact of the matter is, I loved my life pre-cancer. And I think I was living every

02:15:34.460 minute of it. I think I cherished my children. I cherished vacations. I mean, you know, that I

02:15:40.420 cherish travel and showing my children travel. That's a bit of a wonderful thing. And it's also

02:15:46.040 like a dagger too. It's not like I've gotten some new life and new perspective that's so different

02:15:52.260 from my old. Damn it. I liked my old life and I liked the old me. And it's still a little hard to 0.99

02:15:58.780 get used to who this person is now. She's still motivated. She still exercises. Although not

02:16:07.160 doing the things I used to. She loves her children with as much passion as one could have. But I'm

02:16:16.360 fundamentally different. It's tough. Sarah, you've said a lot of things that

02:16:24.360 obviously resonate. And I think will resonate with a lot of people. So I want to thank you from the

02:16:36.880 bottom of my heart and certainly wish you the best. Thanks. I appreciate it. It's been great

02:16:46.920 knowing you through this journey as well. You are, as many of your colleagues have undoubtedly told you,

02:16:53.620 and we've certainly discussed it behind your back. You are an inspiration and nobody wants to hear

02:16:58.560 that because nobody wants to be the inspiration. You just want to be the normal person, but you are

02:17:03.120 an inspiration. I just want to be a normal person. Yeah. Well, thank you for setting aside time.

02:17:09.100 Yeah. And I mean, I thank you so much for having me on. I mean, believe it or not, this is the first

02:17:14.000 time I've told my story in any way, shape or form. So I have been kind of preparing for this

02:17:22.440 and I'm glad I did it. So thank you for giving me an opportunity to do that. And thank you.

02:17:32.060 Thank you for trusting us. Thank you for trusting me and the listeners.

The Peter Attia Drive - April 04, 2022

In remembrance of Sarah Hallberg, D.O., M.S. (Ep. #162 Rebroadcast)

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