The Peter Attia Drive - #162 - Sarah Hallberg, D.O., M.S.： Challenging the status quo of treating metabolic disease, and a personal journey through a grim cancer diagnosis

00:00:00.000 Hey, everyone. Welcome to the drive podcast. I'm your host, Peter Atiyah. This podcast,

00:00:15.480 my website, and my weekly newsletter all focus on the goal of translating the science of longevity

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00:00:41.740 head over to peteratiyahmd.com forward slash subscribe. Now, without further delay, here's

00:00:48.080 today's episode. My guest this week is Sarah Halberg. Sarah is a physician who has spent the

00:00:55.560 better part of two decades focusing on treating patients first with obesity and ultimately

00:01:00.500 really finding her niche in type 2 diabetes. About 10 years ago, she became a huge believer

00:01:06.940 through her clinical experience in the efficacy of carbohydrate restriction and the treatment

00:01:11.040 of type 2 diabetes. And that led to her becoming involved in a company called VertiHealth, which

00:01:16.140 I'm an investor in as well. So I want to disclose that. In this podcast, we talk really about two

00:01:22.040 completely separate things, each of which is important in its own right. In the first part

00:01:26.840 of this podcast, we discuss the role of dietary fat and carbohydrate on the plasma makeup of fatty

00:01:36.420 acid and triglyceride. In other words, does the type of fat you eat play a role in the type of fats that

00:01:43.840 are found in your bloodstream? Because we have a pretty good understanding of what type of fats in

00:01:48.680 your bloodstream are good and bad. How much is that impacted by what you eat? And I think for many

00:01:53.620 people who are new to this area, this will be quite shocking. And suffice it to say, it's not so simple

00:01:59.420 as you are what you eat. And there is enormous implication here, but I think one of the most

00:02:03.740 important takeaways is that one of these fatty acids in particular, which we get into, it's a

00:02:10.720 monounsaturated fat with 16 carbons, turns out to be a very interesting early predictor of metabolic

00:02:18.580 disease. We then pivot off this admittedly somewhat nerdy discussion into perhaps one of the most

00:02:26.000 emotionally riveting discussions I've ever had on the podcast, which is discussing Sarah's personal

00:02:32.760 journey through the diagnosis of lung cancer. She was diagnosed with lung cancer at the end of June,

00:02:39.080 2017. As I discussed in the podcast, it was just a few days after I had seen her appearing to be

00:02:44.880 completely healthy. And to say that the last four years have been anything other than difficult would

00:02:49.940 be an understatement. I don't really want to say more about the second part of the podcast because

00:02:54.840 I won't be doing it justice. I think ultimately it's something that frankly, everyone would benefit

00:03:00.800 from listening to. And it was an admittedly difficult discussion, but one that I feel very privileged

00:03:08.040 to have had with Sarah. So without further delay, please enjoy my conversation with Dr. Sarah Halbert.

00:03:19.940 Welcome to the show. I'm super excited to be speaking with you today. This has the potential,

00:03:26.080 of course, to be a 10 hour podcast, which it won't be, but I think that speaks to the depth of insight

00:03:32.360 that you've got into so many topics that I actually want to talk about. Thank you. It's great to be here.

00:03:37.680 Well, in thinking long and hard about how to navigate all the threads I want to pull on,

00:03:43.100 I figured we would just start with the nerdiest of all topics, which is something that I know you're

00:03:48.120 so passionate about. And yet I don't think gets nearly enough attention. And that is basically the

00:03:56.880 role of dietary intake of both carbohydrate and fats and the relationship that has on the distribution

00:04:04.900 of fatty acids within the body. So let me just start by asking, like, why is that even of interest to

00:04:10.700 you? Well, it's significant interest because it really hits at one of the things people criticize

00:04:17.880 a low carb, high fat diet about is, oh my goodness, you know, you'll get more fat in your muscles,

00:04:26.640 in your liver, and it's going to lead to increased insulin resistance and thereby default going to lead to

00:04:33.720 increased cardiovascular disease. And we know that a therapeutic carbohydrate restricted diet

00:04:41.000 brings down so many cardiovascular risk biomarkers that we're all used to hearing about. Okay,

00:04:48.700 it decreases triglycerides. Okay, it actually can reverse type 2 diabetes in most cases and certainly

00:04:57.380 significantly improve glycemic control in all. But fatty acids, that's not something that's talked

00:05:06.660 about all that often. And what is talked about all that often is this idea of you are what you eat,

00:05:14.760 right? We hear that still every day. Remember, you are what you eat. And this example of what happens

00:05:23.000 when you consume saturated fat in the matrix of a diet that includes carbohydrate restriction

00:05:31.400 is so against that long, worn out idea of you are what you eat. And so fatty acids play a critical

00:05:43.700 role. Study after study will show us in cardiovascular risk and in future diabetes risk as well. But

00:05:52.940 again, it's not discussed because fatty acids are confusing, let's face it, okay? And most people

00:06:00.200 would rather just fall back on this idea, you are what you eat, which just really flies counter to what

00:06:10.140 the evidence in the peer-reviewed published literature says. So maybe taking even a greater step back from

00:06:18.740 that, Sarah, what is it that attracted you personally as a physician towards the management of type 2

00:06:26.960 diabetes? Because, I mean, that's how you and I got to know each other was through a company that you're

00:06:33.060 a big part of called Virta Health, which I'm sure at some point today we will talk about. But what

00:06:38.900 attracted you to this patient population? And how is it that you stumbled upon the idea that there was

00:06:45.500 perhaps another way to treat patients with type 2 diabetes that was not kind of the standard

00:06:52.880 treatment, which was chasing glycemic control with insulin or insulin-increasing drugs?

00:07:01.300 Well, I tell you, it's by accident. If you had told me 20 years ago that I'd be playing this role in

00:07:08.780 the healthcare system, I probably wouldn't have believed you. So it goes back again to the fact

00:07:16.760 that for a very long time, I mean, I've been in the world of obesity care for well over 25 years now.

00:07:24.740 And just the first half of that was telling people that the way to fix everything was to eat a low-calorie,

00:07:32.880 low-fat diet. I grew up as a product of the 80s, like so many people, where that was the dogma. There was no

00:07:41.020 other way. And of course, entering into college and grad school, where I got both my bachelor's and master's

00:07:48.900 in exercise physiology, I mean, that's what we were taught. Moving on to med school, you know, reaffirmed once

00:07:55.700 again. So when I went into practice as a primary care physician, I'm board certified in internal

00:08:02.740 medicine, it was more the same. But again, it was so frustrating to me all along the way, really,

00:08:10.240 to be continually giving this advice and then have people show up being worse. I'm not making them

00:08:17.060 healthier. I'm making them or I'm watching them become more unhealthy. And that was depressing. And it

00:08:24.780 was really quickly became just to the point where it was like, I can't continue on with primary care

00:08:31.940 for the rest of my life because I felt like a legal drug dealer. I got really lucky here. Okay. I like

00:08:39.420 to say a lot of my pivots are pivoted on anger, right? Pivots in my career. And I was really angry at

00:08:46.200 what was happening on the primary care level. And as luck would have it at Indiana University Health,

00:08:52.440 they knew about my background, knew about my past work in obesity care and asked me to start a

00:08:58.560 program, obesity program. And I jumped at the opportunity. And I was lucky to be able to take

00:09:05.440 some time off over the next year, spend time figuring out what was this going to look like?

00:09:11.680 How are we going to tackle the untackleable, if you will, problem, you know, that is obesity.

00:09:17.500 And I started sticking my nose in the literature, which is something that every physician wants to

00:09:24.780 do. But not every physician is afforded the time. Let's face it, you know, we are just boom, boom, boom,

00:09:33.180 see patients. There's just such a busy lifestyle in everything right now. But I was given a chance to

00:09:39.280 step back some. So I had time to prepare for this. And in that, I discovered carbohydrate restriction.

00:09:47.220 As a means to weight loss initially. Listened to some lectures by Dr. Steve Finney and Jeff Fulick.

00:09:55.640 And I was like, whoa, that makes total physiologic sense. And so boy, did I dig deeper into this.

00:10:03.780 I read everything I could get my hands on, and really came to the conclusion, which required a lot

00:10:11.460 of cognitive dissonance overcoming, that what I had been saying for well over a decade to so many people

00:10:20.320 was really not founded on good science. And that the field of carbohydrate restriction,

00:10:28.860 while still relatively in its infancy at the time, showed much more promise. And so we opened the

00:10:37.120 clinic as a carbohydrate restricted clinic. But the fact of the matter is, although people were losing

00:10:43.640 weight, what we were seeing that was so much more meaningful was that people's diabetes was like going

00:10:50.780 away. They were having normal blood sugar. We were pulling them off of insulin at rates that I could

00:10:57.760 never have believed had I not been the physician who was taking care of these patients. I was

00:11:03.620 astronomical. Hundreds of units of insulin. First of all, there's two questions I guess I

00:11:08.600 want to ask you. One, were these patients primarily patients with type 2 diabetes, or was it primarily

00:11:12.940 obesity, of which a subset had diabetes? And secondly, how much resistance did you have in your own

00:11:18.700 institution when you showed up and said, hey, I know you guys brought me in to do this thing. I'm going

00:11:23.980 to do it. But oh, by the way, my secret sauce is going to be this, at the time, very unconventional

00:11:29.180 approach. As you probably can imagine, when patients come into an obesity clinic, most all of them,

00:11:36.620 if not all of them, have some form of metabolic disease. The biggest being type 2 diabetes. So we

00:11:43.480 were seeing type 2 diabetes all of the time, consistently daily. And you're right, I had to

00:11:50.700 take precautions. Because again, this was 10 years ago. And not as much about carbohydrate restriction

00:11:59.240 was known at that time, certainly among general practicing physicians in any discipline, really.

00:12:06.860 And so I knew that I had a head off the potential resistance that was going to come. There was just

00:12:13.480 no question of it. So I actually went about and spent an entire summer meeting with all the departments

00:12:21.740 in our local med center, and giving them a 15-minute slide presentation of when your patient comes back,

00:12:32.040 says that Dr. Hallberg told them to eat a lot of fat and not a lot of carbohydrates, that I wasn't crazy,

00:12:38.420 that this was actually based on evidence. And here it was. And you know, Peter, you'd be surprised.

00:12:45.220 I didn't get any pushback. I actually pushed it even to the next level. I was part at that time of the

00:12:52.240 Ambulatory Quality Committee at our institution. And I actually brought up an amendment that all

00:12:59.620 patients with metabolic disease should at least be provided the option of trying this if they wanted.

00:13:08.420 And it passed unanimously. I mean, people got it. Once they had time to pause, take a look at the

00:13:14.920 physiology behind this and realize, okay, yeah, that makes a lot of sense. So it changed my life,

00:13:22.200 right? And again, I like to always say my career is built of inflection points of anger. And as we

00:13:29.100 were seeing these huge changes of diabetes and patients just resolving their diabetes, I became really

00:13:37.340 angry because I was like, where is this? Where's this in the guidelines? How come I've never heard

00:13:43.060 of this before? I mean, this is, I mean, I hate to be like overdramatic, but it truly is quite miraculous

00:13:49.640 for a disease that everyone thought was chronic and progressive to see people recover from it.

00:13:56.280 It's quite astounding. And so I decided that I needed to get into research. So actually to start

00:14:05.720 off with, I called Purdue University's nutrition program and asked one of the researchers there if

00:14:11.980 they wanted to help me on just an early unfunded pilot study to prove my point, looking at metabolic

00:14:18.180 improvements and looking at financial improvements too. Because obviously if people weren't taking all

00:14:24.840 this medicine, they weren't costing themselves and of course the healthcare system as a whole as much

00:14:31.040 money. So I talked about that study, presented it at the National Lipid Association quite a long time

00:14:37.440 ago, talked about it actually in my TED talk, and then was speaking at the Obesity Medicine Association

00:14:46.600 quite a long time ago and actually met Dr. Steve Finney. And that really changed the course

00:14:54.700 of my life as well. So all this time you're sort of putting into practice what Steve and Jeff had

00:15:01.160 been writing about for a long time. And obviously Steve is someone I've been dying to have on the

00:15:06.480 podcast and we were actually supposed to do it at one point in time and then scheduling got in the way.

00:15:11.980 But I didn't realize that you had already sort of gone down this path and yet hadn't actually met him

00:15:18.300 because I took the opposite approach, which was when I started kind of implementing some of these

00:15:22.560 treatments. I'm just a bull in a china shop. I just reached out to Steve right away.

00:15:27.340 I might have been one of the first people to get a copy of the book that he and Jeff wrote in 2011.

00:15:32.340 I think I got a preprint of that book, which I still have, by the way, the art and science book,

00:15:37.280 which I have. It might have more highlights and post-its in it than any book I own.

00:15:41.580 Because I think like you, I was kind of going through the, this can't be. There's something so

00:15:47.540 counterintuitive to this that I need to read this over and over and over. I'm going to make sure I get it.

00:15:52.160 So it's funny that that's the case. Now, tell me, where did, you know, were you at this time going to

00:15:57.020 ADA meetings, the American Diabetes Association meetings? And when you would discuss what you were

00:16:02.600 seeing in your practice with your peers who were also on the front lines taking a more traditional

00:16:08.320 approach, how was your experience being, how was that met? Well, it's interesting. If I was speaking

00:16:16.060 with someone who took care of obesity patients for obesity, they were totally, I get it. I'm doing

00:16:28.920 the same thing to some varying degree. But when you moved out of that space to other subspecialists,

00:16:37.000 the first thing was, oh yeah, their diabetes will go away, but you're going to kill them with heart 0.86

00:16:42.300 disease. Right. Or, oh, you know, we all know it works. I'll never forget one of the leaders in 0.88

00:16:49.700 the endocrine movement said, look, we all know it works. This is not a secret, but nobody can stay

00:16:55.320 with it. And I was like, you know, I don't know here in my practice, I have thousands of patients

00:17:01.740 that would beg to differ with that. And so, you know, those are the feedback that I got. And one of the

00:17:08.080 things was I knew that there had to be even more research done. I mean, you know, we had wonderful

00:17:13.340 pioneers in Steve and Jeff and Eric from Duke, Westman, but we needed even more. They needed to

00:17:22.140 be larger trials. They needed to really specifically focus on patients with type 2 diabetes because I was

00:17:27.760 convinced almost from the get-go that that is the target population here because that's where we see

00:17:35.340 the biggest improvements. So this chance meeting with Steve at Obesity Medicine Association conference

00:17:42.840 led to a dinner and led to funding of the large clinical trial that we're actually wrapping up

00:17:51.480 in the next couple of months. Right now, we're at the tail end of our five-year data collection

00:17:56.520 of the longest and largest trial looking at nutritional ketosis as a means of reversing type 2 diabetes.

00:18:05.340 And prediabetes, which I'll just kind of stick in really quick here. Today actually happens to be the

00:18:13.180 day that the prediabetes paper was published. So I'm really proud to say this is the eighth paper

00:18:20.420 already that's come out of this large trial, started by a chance encounter at a conference.

00:18:27.820 We haven't published the prediabetes results until today. So this was a paper that looks at the first

00:18:34.700 two years of prediabetes, utilizing remote continuous support to help patients adhere to a diet aimed at

00:18:45.620 nutritional ketosis. And Sarah, these are patients defined as prediabetic by hemoglobin A1c?

00:18:53.200 Correct. And that's being defined as 5.7 to 6.4? Is that the range?

00:18:58.640 That's correct. Yes.

00:19:00.420 Okay. Tell people what that means. I think most people are aware of what a hemoglobin A1c is, but

00:19:06.160 what does that translate to in an average glucose approximately?

00:19:10.660 Yeah. So we really start to get, for example, fasting. That's the one most people are familiar

00:19:15.240 with. And once you get a fasting glucose over 110, that's the worrisome prediabetes range.

00:19:22.920 And I do have to say here, though, that doesn't mean normal glucoses are okay for everyone. And I

00:19:31.600 think you've had, you know, many people on here talking about the perils of insulin resistance and

00:19:37.660 how it starts to cause significant problems in people who still have normal blood sugars. And I

00:19:44.240 just think that's such an important point and can't be overstated again. But in this study,

00:19:50.040 we're looking at people who had insulin resistance long enough that their pancreas and the beta cells

00:19:58.020 could not keep up with the insulin that was needed to keep blood sugar normal. And their blood sugar

00:20:05.200 started to rise, not yet to the level where a diagnosis of type 2 diabetes could be made. But

00:20:14.040 once again, where we see the impact of insulin resistance affecting the body's ability to keep

00:20:23.580 blood sugar normal due to pancreas being overworked for far too long.

00:20:30.720 And if we believe that, I mean, I don't know what the latest numbers are, but I'm guessing it's still

00:20:36.380 about 10% of the US population has type 2 diabetes. Is that approximately correct? Or is it, are we more

00:20:42.380 than 10% now? Approximately, with also the caveat of much more concerning levels in different minority

00:20:50.440 populations, which of course, hopefully we'll get a chance to talk about later, is just a huge goal

00:20:58.940 with improving health equity in this country. So if it's 10% in all comers, do you have a sense of

00:21:05.160 what it is in Hispanic and African American populations? Yeah, it gets even higher. It's

00:21:09.660 well into the teens and those in Pacific Islanders as well. So these are populations that, you know,

00:21:15.860 we need to be paying attention, of course, to everyone who has type 2 diabetes. But we also need

00:21:20.960 to be paying attention to who's at greater risk. So what percentage of the population do we believe

00:21:27.920 is formally in the pre-diabetic camp? Which again, I think what you said a moment ago is very important

00:21:33.880 for people to understand. If we go back to the podcast with Jerry Shulman, which is one of my

00:21:38.740 favorite discussions ever on the topic of insulin resistance. I mean, Jerry really laid out elegantly

00:21:43.900 the long time course of this disease. And even if you have normal fasting glucose and fasting insulin,

00:21:52.600 but that early sign of elevated postprandial insulin is really that early sign of insulin resistance that

00:21:59.180 will then lead to postprandial glucose elevations. And even that can still exist in the presence of

00:22:05.180 normal fasting glucose. So to your point, by the time someone registers as a pre-diabetic,

00:22:12.080 quote unquote, I mean, this has been a process that's been going on for five to 10 years.

00:22:17.440 What is our belief about how many or what percentage of Americans, just to make it

00:22:21.260 American centric for a moment, what percentage of Americans are in that bucket?

00:22:25.240 Well, I tell you, recent studies will show us that over 50% of Americans, adult Americans,

00:22:31.160 have diabetes or pre-diabetes. And a study released a couple of years ago, and I mean, this should shock

00:22:39.700 everyone to its core, based on NHANES data, that 88% of Americans are not in optimal metabolic health.

00:22:49.960 I mean, let me say that again. 88% of adult Americans are not in optimal metabolic health.

00:22:57.300 And that is by looking at NHANES data and taking a look at the criteria for metabolic syndrome.

00:23:04.920 And so the 12% are those who didn't meet any of the criteria for metabolic syndrome. I mean,

00:23:11.880 that's frightening. Yeah. So I was going to ask you if that's exactly what it meant. So

00:23:16.020 just let's state for the listener what metabolic syndrome is. We've certainly discussed it on this

00:23:21.140 podcast, but it would be great to remind people, what are those 12% doing? They have none of the 0.96

00:23:27.220 following five, right? They have normal blood pressure, though they do not have elevated blood

00:23:32.040 pressure. And they're not on medication. And they're not taking medication to lower blood

00:23:35.940 pressure. And normal is now being much more stringently defined. But I believe the latest

00:23:40.720 CDC definition of normal is less than 130 over 80. In our practice, we advocate less than 120 over 80.

00:23:49.760 They have normal fasting glucose, and that's defined as less than 100. They have normal triglycerides,

00:23:57.440 which are being defined as less than 150. We argue in our practice, that's very high. And anything 0.87

00:24:03.540 over 100 is elevated. They have normal HDL cholesterol, which for men is defined as greater

00:24:10.540 than 40 milligrams per deciliter, for women greater than 50 milligrams per deciliter. And they do not have 0.93

00:24:17.440 truncal obesity. And I forget, I think for men that's defined as 40 inches of waist circumference and

00:24:23.880 women 36. I don't know if that's still the latest. Well, yeah. And I will also point out one really

00:24:29.820 important thing here when it comes to waist circumference too, and the definition of metabolic

00:24:36.600 syndrome. And it little bit goes back to what I was saying before about the consideration of minorities

00:24:43.200 and different ethnic populations, which is we have to take that into account, even when we're defining

00:24:53.160 metabolic syndrome. Because for Southeast Asians, they are defined as having metabolic syndrome at a

00:25:02.340 much lower waist circumference. And for African Americans, we need to really consider as well,

00:25:08.800 because they tend, even in the face of having insulin resistance, they tend to have normal triglycerides

00:25:17.280 and HDL. And so again, we can't be treating everybody the same, but we often do.

00:25:26.800 Yeah. I'm glad you pointed that out. I still remember it was about 10 years ago when I learned

00:25:32.480 that lesson, which was taking care of an African American patient who had about the most uncontrolled 0.81

00:25:39.440 diabetes I'd ever seen. You know, hemoglobin A1C of 14%. This is a person who's basically going to have

00:25:45.640 their limbs amputated in the next hour. Triglycerides of 89. Just, yeah, just totally normal. You look at

00:25:53.600 their lipid panel, you wouldn't think anything is wrong. Right. And so that's the thing is they can

00:25:58.660 get missed. And so knowing this and educating people on things like this, again, goes back to our working

00:26:05.500 on health equities. And it's so important and so often not something people take into account. And just

00:26:12.880 going back to prediabetes, the most frustrating thing, I shouldn't say that. It's one of the most

00:26:19.980 frustrating things. There are many things about our healthcare system I could enter into the most

00:26:24.840 frustrating. But one of them is patients coming in to see me whose lab showed prediabetes. And I said,

00:26:33.980 oh, you have prediabetes. Oh, no, no, no. My physician said I was fine. The fact that we don't appreciate

00:26:40.000 that by the time you get to prediabetes, there's some really serious things going on here. Their

00:26:47.280 vision is being impacted. Their nerves are being impacted. You know, these are things we can't just

00:26:53.880 say, oh, they haven't gotten bad enough to bother with because they're not at the criteria for type 2

00:27:01.640 diabetes yet. I mean, we have to pay attention. And so that's one thing. If there's any physicians

00:27:08.480 listening, which I know that there are, don't ignore any elevation in blood sugar. That means

00:27:16.240 there's been a problem for a long time already. And patients should be also hypervigilant about this.

00:27:22.700 I mean, I've seen patients in that prediabetic camp, and this is using an example of a male patient,

00:27:28.760 when their insulin sensitivity is restored and their blood glucose comes down by an average of 10

00:27:34.600 milligrams per deciliter, they'll say, wow, I have better erections all of a sudden. And that speaks

00:27:40.260 to even the microvascular damage that's being done long before you get to diabetes. You know, I actually

00:27:45.200 was exchanging emails with a really good ophthalmologist recently and kind of trying to ask how far are we

00:27:53.000 away from being able to use retinal imaging as a screening tool for early, early, early microvascular

00:28:02.420 disease. Because I think the hemoglobin A1C is just far too crude a metric for this. And I actually have

00:28:08.480 seen some interesting literature, and I'm sure you've seen even more of it, that suggests that this is, you

00:28:13.160 know, if you look at the microvasculature in the eye, it might be one of the earliest warning signs of when

00:28:19.440 things go awry. And so in an ideal world, I would love it if, you know, we had tech that basically allowed for

00:28:26.400 quick and easy evaluation of that. So that to your point, it doesn't really matter if your trigs are up

00:28:33.580 or down and your waist is big or not. Like, let's look at the actual place where the damage is taking

00:28:38.960 place and make the assessment on an individualized basis, as opposed to using these sort of population

00:28:43.980 based metrics, which move in the right direction, but for any one individual can be quite misleading.

00:28:48.300 Yeah. And then I love the eye discussion because, you know, one of the other, I think, really important

00:28:54.960 questions is, once we do get to damage, can we make it better? Can we make it better without and skip

00:29:04.000 some of the horrors of having diabetic eye disease for millions of patients? I mean, that is a really

00:29:13.280 burning question for me and one that I think we need to really explore. Yeah, indeed. So with that

00:29:23.540 background, let's kind of dive into some of this nerdy, nerdy fatty acid stuff. And I got to tell

00:29:31.180 you, I find this stuff really interesting in part because I think it's complicated enough to make sense

00:29:39.920 of just the eating side of this stuff. In other words, I think people that have listened to this

00:29:46.620 podcast, we've done a number of shows that have dealt with fatty acids. People probably understand

00:29:51.260 that there are saturated fats, monounsaturated fats, and polyunsaturated fats. The saturated fats

00:29:57.220 have no double bonds. So that means every carbon is fully saturated with hydrogen. The monounsaturated

00:30:04.320 have one and only one unsaturation. So one double bond. And then the polys have at least two of these

00:30:13.140 double bonds. But it's the manner in which these things can be made from each other that becomes

00:30:19.160 quite interesting, isn't it? It's really the way that you can ingest one form and it can be turned

00:30:24.940 into another. So I'm wondering if the easiest place to begin this discussion is to introduce

00:30:33.160 what the fate of a very common fat in our body is, which is the C16 saturated fat. So can you talk a

00:30:45.800 little bit about how abundant that is and what our body's options are for it? What it's called,

00:30:51.480 let's start with the nomenclature. What does pure C16 look like?

00:30:54.940 That's palmitolytic acid. So it's really interesting what happens. And do you mind if I

00:31:00.660 jump on and share screen here so we can talk a little bit more about it?

00:31:05.920 Yeah, that would make it easier for everybody, I'm sure.

00:31:07.940 I want to start by talking about saturated fatty acids in general. And what we know is that going

00:31:17.900 back here to the basics and looking at the liver, when we have incorporation of saturated

00:31:24.740 fatty acids into our triglycerides, that is correlated with insulin resistance and adiposity,

00:31:33.120 likely reflecting accelerated hepatic de novo lipogenesis. Or also it can be what is actually

00:31:40.460 returned to the liver. So really two. We certainly know that hepatic de novo lipogenesis is a big part

00:31:49.660 part of the problem when it comes to elevated triglycerides, but we can also make these with

00:31:56.660 some what is delivered exactly back to the liver. And so when we see saturated fatty acids as a makeup

00:32:05.360 of triglycerides or maybe even the phospholipids there, we say, oh my goodness, that's a marker of

00:32:13.680 increased saturated fatty acid consumption, right? These people are eating a high saturated fat diet.

00:32:22.340 And that seems to make sense. And this is the problem with a lot of things in science in general,

00:32:28.780 and nutrition science is no different, is that just because it seems to make sense

00:32:34.000 doesn't mean it's the way things actually work.

00:32:37.640 Sarah, can I explain a technical point on this slide that you and I will take for granted,

00:32:42.900 but I want to make sure that a listener understands. So when a patient goes and gets their blood drawn,

00:32:49.100 let's just say they get a standard lipid panel. It will spit out the following values. Total

00:32:55.080 cholesterol equals 200 milligrams per deciliter. LDL cholesterol equals, you know, 140 milligrams per

00:33:03.180 deciliter. Triglycerides equal 150 milligrams per deciliter. HDL cholesterol is 35 milligrams per

00:33:10.360 deciliter. And VLDL cholesterol, if I remember the numbers I just spit out, would be 25 milligrams per

00:33:16.420 deciliter. In other words, the VLDL cholesterol, HDL cholesterol, and LDL cholesterol sum to the total,

00:33:22.100 and then the triglycerides are independent. What I want to make sure people understand is

00:33:26.840 those are all found within the lipoproteins. So VLDL cholesterol is the amount of cholesterol

00:33:37.340 ester contained within the very low-density lipoprotein. LDL cholesterol is the total content

00:33:43.540 of cholesterol ester found within the low-density lipoprotein, et cetera, for the HDL. Here's the part

00:33:50.580 that's really interesting. We always check these things fasting because when it comes to measuring the

00:33:56.520 triglyceride, we want to eliminate what's in the chylomicron. We want to eliminate the immediately

00:34:02.040 absorbed triglyceride from the gut. And by doing that, we basically capture what you have on this

00:34:08.960 photo. When we measure a triglyceride, for all intents and purposes, we are basically measuring

00:34:16.060 the 90% of triglycerides that are captured within the VLDL. So let me restate that because that was a bit

00:34:22.500 rambling. When you go to the doctor and get your blood tested and it says your triglycerides are

00:34:27.640 150 milligrams per deciliter, that's basically saying, look, 90% of that 150 milligrams per

00:34:33.980 deciliter is within your VLDL cholesterol. Some of that is in intermediate-density lipoprotein,

00:34:39.780 but that's virtually non-existent. There's a trace of that in the LDL cholesterol and even a smaller trace

00:34:45.500 in the HDL, but the lion's share is in the VLDL cholesterol. And as you're going to explain to us,

00:34:52.880 this process of de novo lipogenesis, the conduit from fat being made in the liver and exported,

00:35:00.000 that conduit is the VLDL particle. That's going to become very important in this discussion.

00:35:04.860 Absolutely. Yeah. And that's really important. Thank you for the precursor explanation because

00:35:09.920 this is technical stuff and that is really important for people to understand. Then the

00:35:16.460 next question really becomes, okay, so if we have a high saturated fatty acid content within the VLDL,

00:35:27.900 okay, again, it's being in the triglycerides, the phospholipid membrane, wherever we find it,

00:35:35.920 where did the saturated fatty acids come from? Is it directly from consumption? And I just want to

00:35:46.060 first point out before we get into maybe more of the technical stuff, some of the clinical trials

00:35:52.080 that can help us understand this a little bit better. And so this is one of my favorites by Dr.

00:35:59.780 Brittany Volk that was published a while ago. And it's really great because this was a

00:36:05.880 feeding study. So, you know, they kept track of what the patients were eating. It wasn't a free for

00:36:11.720 all. Are they eating what they were telling them to eat or not? They provided all of their food.

00:36:19.120 And this was patients with metabolic syndrome. They went through six feeding phases. And so they did a

00:36:27.220 run in with a very low carbohydrate diet for everyone, less than 50 grams of carbohydrates a day.

00:36:34.000 And every three weeks, they increased the carbohydrates in the diet, all the way up to

00:36:42.020 346 grams, which was C6 feeding phase. And the other thing to note here is the saturated fat content.

00:36:51.920 So when we were at the low carbohydrate end here in C1, they were consuming 84 grams of saturated fatty

00:37:00.860 acids a day. Okay. So that blows away any guideline on saturated fat. I mean, so far above what anyone

00:37:10.120 would consider at goal. And then we get down to the C6 and we're much less 32 grams. Again, what happens

00:37:20.040 to the fatty acids as people are run through these six phases?

00:37:25.380 And Sarah, just to be clear, this is basically an isocaloric feeding study, which means as you're

00:37:33.300 ratcheting up the content of carbohydrate, you're commensurately reducing at a caloric level,

00:37:42.680 the amount of saturated fat, right? I believe this study did not change the number of calories they

00:37:47.580 were consuming. Correct. They did not. And so what happened over these six phases? So here we have

00:37:57.020 saturated fatty acid levels marked. Okay. So here's the baseline at that run in. And we see when we have

00:38:05.400 the very high saturated fat level, very low carbohydrate. Here we go. And what's really

00:38:13.060 interesting is what happens as we march along here down to C6. And if you remember, this is much

00:38:20.620 lower saturated fatty acid content of the diet, much higher carbohydrate intake. What we see is that

00:38:31.180 it's actually the saturated fatty acid content is actually higher with the lower saturated fat intake.

00:38:40.060 And we're going to come back and talk to about the science behind that. But I think it's really

00:38:44.780 important for people to see this clinically. And then maybe when we get into a little bit more of the

00:38:50.580 nitty gritty, it can make more sense. I mean, it's actually statistically insignificant in terms of C16,

00:38:58.880 right, which is the dominant saturated fatty acid. So palmitic acid, it trended towards an increase

00:39:06.320 as saturated fat, dietary saturated fat went down and carbohydrate went up, but it didn't reach

00:39:13.880 significance. And the only one that actually did significantly increase was C14, right?

00:39:21.800 Yeah. Actually C16-1 as well. And that one is we're going to spend hopefully a little bit of time on.

00:39:28.840 Yeah, yeah, yeah. No, but as a saturated fat, it was really just-

00:39:31.700 Oh, as a saturated fat, yes. Yeah, yeah, yeah.

00:39:33.920 But the point of this is we didn't have these really high levels of serum saturated fatty acids

00:39:43.420 when we were consuming, when these participants were consuming this very high saturated fat diet.

00:39:51.280 Essentially, and this is important, it stays the same. If anything, there's a trend

00:39:56.420 to higher serum saturated fat in the low fat arm, okay, but certainly we do not see a rise in the

00:40:09.120 high intake of saturated fat. That's super important. And again, it goes against what I was

00:40:16.280 saying earlier on. You are what you eat. Well, okay, if that's true, then when I consume a very high

00:40:24.940 level of saturated fatty acids, why am I not seeing that, again, in the blood, in the serum? Why are we

00:40:34.560 not seeing that? And what's nice in this study is you've exhaustively looked at where the fatty acids

00:40:43.080 are. So obviously the most efficient place we store fatty acids is in the triglyceride, but you also store

00:40:50.440 it within the cholesterol ester. And it's obviously in the phospholipid as well. But regardless of where

00:40:58.560 you look, you see no association between dietary saturated fat and fatty acid composition with

00:41:07.480 respect to saturated fat. That's right. That's right. And I want to really quick draw attention here to

00:41:13.920 one more that we are going to be talking more about. And that's 16-1. That's palmitoleic acid. And we're going

00:41:24.660 to talk more about why that's important. But as we can see here, when we follow that across, it significantly

00:41:33.400 rises when we have less saturated fat and more carbohydrates. And you can see that is statistically

00:41:41.220 significantly different in every place that we're looking. So moving on, one other trial that shows

00:41:51.680 this. And then we'll bring up the table that I had erroneously brought up for the first study. But

00:41:57.680 when we take here a low saturated fat diet, low fat, low saturated fat diet, and we compare it to a low

00:42:07.540 carbohydrate, high saturated fat diet over 12 weeks. This is from Jeff Volick's group from 2008. And what I like

00:42:17.320 here is you can see very readily with these pie charts, exactly what the content of the two diets were. So

00:42:25.520 again, we really have it flipped, high carbohydrate, low carbohydrate, low fat here on the left, to a very high

00:42:35.400 intake of fat on the right. And again, below it, the two different levels of saturated fat that we're

00:42:43.160 comparing. 12 grams to three times as high in the low carb diet at 36. These are both really low calorie

00:42:53.300 studies. Was this an ad lib feeding study or were these deliberately calorie restricted? How was this

00:42:59.660 study done? Yeah, these were both that wanted the calorie intake of the two studies to be the same.

00:43:05.680 So as you can see, they're about 1500 calories a piece. And were they deliberately calorie restricted?

00:43:11.600 Yes. So what we can see here is that what we have when we take a look at these two arms is taking a look

00:43:22.180 on the right to the change in serum saturated fatty acids. We can see in the carb restricted diet,

00:43:29.860 significant decrease versus the low fat diet. So again, in the much higher saturated fatty acid arm,

00:43:39.620 we see a significant decrease down. Whereas we do see a drop in the low saturated fatty acid intake group,

00:43:48.120 but not nearly as much as we see with the carbohydrate restricted group. Once again,

00:43:55.460 arguing against you are what you eat. And I want to now get in a little bit more to this,

00:44:03.060 what I think is actually even more important, which is the change in the palmitaleic acid.

00:44:09.640 Yeah. So palmitic acid is 16-0. Palmitaleic acid is 16-1. They look almost the same,

00:44:17.340 except that palmitaleic, the 16-1 has that double bond at the N7 position. And you're going to

00:44:25.700 explain in a moment, which enzyme does that and why that matters, right?

00:44:30.440 Right. Absolutely. You know, what is it about this? It's not a saturated fatty acid. So why do we care

00:44:36.240 so much? What happens to 16-1? But it's pretty evident here what happens first of all, and then we'll

00:44:43.440 talk about why. What happens is that with 16-1 in the high saturated fatty acid group, it drops

00:44:52.380 significantly. Where in the low fat group, again, low saturated fatty acid group, it actually goes up.

00:45:01.080 And this is a statistically significant difference. Okay. Much more significant, even as we look,

00:45:08.520 than the change in the serum fatty acids. So now I'm going to pull up a graph of these results to look

00:45:17.460 at it a little better. And then I want to get into the actual science of it. This is the very low

00:45:24.360 carbohydrate arm on the left, and it is the low fat arm on the right. And so what we see here,

00:45:33.600 when we look at total saturated fatty acids, is that it has dropped 5% between the low carbohydrate

00:45:44.040 group and the low fat group, total saturated fatty acids. What about the 16-1? And what we see here

00:45:55.940 with the 16-1 in much more significant statistically is that we see between a low carbohydrate diet and a

00:46:06.860 low fat diet, that we have a more significant decrease in the 16-1 with the low carbohydrate,

00:46:18.840 higher fat diet. So there's a couple of things going on here for people that are going to be

00:46:24.480 overwhelmed by this table. And I apologize if you're just listening to this without watching

00:46:27.840 it on video, I'll do my best to explain what's going on here. So the first thing to notice here

00:46:33.100 is both of these groups of patients started out with quite elevated triglycerides. So in the first

00:46:40.060 group, in the group that was randomized to the very low carbohydrate diet, their average triglyceride

00:46:46.420 at the start of this study was 211 milligrams per deciliter. That's sky high. At the end of 12 weeks,

00:46:52.620 it was down to about 104 milligrams per deciliter. It fell by about 50%. Conversely, the group that

00:47:01.540 started out in the low fat arm, also very high triglycerides to start, 187 milligrams per

00:47:07.860 deciliter. By the end of 12 weeks, they saw about a 20% reduction to about 150 milligrams per deciliter.

00:47:15.600 Now this is where these tables get a little bit confusing because the table is showing both

00:47:21.280 the relative and absolute reduction of the relative or constitutive fatty acid. In this case,

00:47:29.240 16-0 and 16-1 and 7, the two we're talking about. What does that mean in English? It means that when

00:47:36.120 you look at the total amount of saturated fat reduction on a relative basis, both groups saw a

00:47:43.620 slight reduction, but it was statistically more significant in one group than the other. The low carb

00:47:49.560 group was a 12% reduction versus 5% in the low fat group. And on an absolute basis, that difference

00:47:57.400 was even greater because the low carb group had such a significant reduction in total triglyceride

00:48:04.420 as well. And that's the dominant source of where you're going to see these fatty acids. And of course,

00:48:08.900 the reverse is true when it comes to 16-1. So let's now ask the question, Sarah, what is it about

00:48:19.400 palmitolaic acid that you think is such an important biomarker? Because we wouldn't be having this

00:48:25.980 discussion if you didn't think we should be paying attention to this.

00:48:29.580 I think it's a really important biomarker. And if you would allow me, let me point out one other

00:48:34.640 thing here regarding the triglycerides, because clearly the low carbohydrate arm decreased more

00:48:42.420 in the triglycerides. The low fat arm decreased too, which may come as a surprise to your listeners

00:48:51.240 because we do associate low fat with an increase in triglycerides. But I do want to remind everyone

00:48:58.620 that this was a calorie restricted, that this was around 1500 calories. So that drop in the low fat

00:49:06.900 diet arm, although maybe not what we were expected, does make sense with the reduction in calories

00:49:13.780 overall. Now, let's go back and talk more about your question, okay? I think palmitolaic acid, or again,

00:49:23.640 that's that 16-1, is really not appreciated as the health predictor that it really is, okay? So let's

00:49:36.580 go through, I'm going to just jump ahead a little bit here. So palmitolaic, or we like to call it POA,

00:49:44.620 is a product of something called sterol-CoA desaturase. And sterol-CoA desaturase is going to

00:49:55.400 determine what is going to happen with some of the fatty acids in our system, specifically what's going

00:50:05.660 to happen to POA. Now, what we know ahead is that sterol-CoA desaturase is actually an independent

00:50:15.300 marker of triglyceridemia and abdominal adiposity. So in other words, an independent marker of all those

00:50:23.140 things that go along with insulin resistance. So if we have high levels of sterol-CoA desaturase

00:50:31.580 activity, right there, we got to start thinking things may be concerning, even if someone has

00:50:40.040 a normal blood sugar, right? Because right now, I think one of the important things based on

00:50:45.860 the earlier part of our conversation, where we say so many times these things are missed,

00:50:51.420 people can still have normal blood sugars, it's going to be really important, you know, number one,

00:50:57.180 that we make everyone aware that a normal blood sugar doesn't mean that you are healthy. But number

00:51:03.340 two, what are some easy ways and some easy markers, maybe that we can check to know that we're headed

00:51:10.200 for trouble, even before we have blood sugar go up. So plasma triglycerides, and let's take a look

00:51:19.520 at, again, POA in those plasma triglycerides in the way of looking at it in core tiles. So again, low

00:51:30.640 versus high. And what we can see is the POA, the byproduct of sterol-CoA desaturase is much higher,

00:51:42.600 the higher the triglycerides are. Very important. So if your triglycerides are really high,

00:51:49.420 again, what's happening very likely is that your POA is elevated as well, brought about by increased

00:51:59.220 activity of sterol-CoA desaturase. And this shouldn't be surprising, right? Because if you look

00:52:08.320 at the very unfriendly diagrams of fatty acid metabolism, one of the first steps we see in the

00:52:18.040 conversion or elongation of fatty acids is the conversion of C16-0 palmitic acid into C16-1

00:52:29.720 palmitoleic acid N7 through an enzyme that has two names, I guess, depending on the name and

00:52:35.760 nomenclature, right? So delta-9 desaturase, desaturate the number nine carbon from the delta

00:52:41.740 end, also known as sterol-CoA desaturase, which I think is the more popular name is SCD-1, right?

00:52:48.860 Right.

00:52:49.620 And if you go down that pathway, what you're basically doing is bundling and packaging fat

00:52:55.880 to leave the liver, right?

00:52:57.920 Yes. And here is one of the, that is an interesting point because the question is if we're trying to

00:53:05.360 change the serum saturated fats into something else, I mean, the body is obviously doing that,

00:53:14.580 one would have to wonder, is that a protection mechanism? Why do we want to do that?

00:53:21.160 To me, that's a great question, Sarah. It seems counterintuitive if I'm going to be obvious because

00:53:25.800 we would think that a saturated fat is much safer. It's inert. There's no chance a reactive oxygen

00:53:33.100 species can be formed out of it. Why is it our body, even if we wanted to export fat from the

00:53:38.560 liver, which we could argue all the reasons that's not a great idea, why would we go to the trouble of

00:53:43.420 this conversion? All right. Well, let's go through it really quick and then get to answering that

00:53:48.860 question because I think it's really important and really sheds light on why we need to be paying

00:53:55.820 more attention to the all-important POA and, of course, the precursors and

00:54:03.100 enzymes that act in its creation. So let's go through, if you will, this cartoon that I know

00:54:09.980 looks really busy initially, but let me just kind of run through it starting here in the intestine.

00:54:17.940 And remember, you know, we'll start off by saying our focus in health care and in nutrition

00:54:23.620 recommendations for so long has been low fat, low fat, more carbohydrates, higher carbohydrates.

00:54:30.240 Well, let's take a look in the intestine at those carbohydrates, changing the focus for a minute.

00:54:37.600 So they come in rapidly absorbed carbohydrates or even our slowly absorbed carbohydrates,

00:54:43.880 our starches, okay? And what happens when they come in? As glucose, that feeds in again through

00:54:52.160 GLUT2 into the pancreas, pushing out more insulin. Insulin then feeds into the liver. And what we get

00:55:03.140 here is going through a big, big part of this is SREBP1, okay? And I don't know if we need to get that

00:55:13.040 technical, but we'll lead here to that enzyme we were talking about, the SCD1 or sterile CoA desaturase

00:55:23.840 increasing. Very important. And it comes about through other means as well. Fructose coming in

00:55:31.100 through GLUT5 or glucose coming directly into the liver through GLUT2. They're all feeding into this

00:55:40.000 by slightly different mechanisms to increase this SCD1. Now we're going to look more at the process

00:55:50.760 in a different way. So we have increased hepatic, first of all, saturated fat. Okay, here's our 16-0,

00:56:01.480 the saturated fat. Increase hepatic levels of this. What gets turned on as from the past cartoon,

00:56:11.120 we get that SCD1 activity increasing that leads to this increase in POA. Coming down here,

00:56:24.920 what's the end gain here? Increased VLDL. Same thing over here, looking at it different. We see again,

00:56:37.560 SCD1, if it's blocked, we won't see that. We'll see a decrease in VLDL. And this again has to do,

00:56:47.940 if this SCD enzyme is blocked, we're going to have an increase in the saturate, a decrease in our POA.

00:57:00.740 But again, what we have when we're consuming the high carbohydrates, even if they're the, again,

00:57:10.280 more refined carbohydrates or the less rapidly absorbed carbohydrates, this is the path that we

00:57:18.160 wind up going on. 16-0, saturated fat is elevated and it turns on this cascade leading to increase

00:57:29.300 in VLDL. Yeah. Again, I think for folks that are watching this, it's going to make a bit more sense.

00:57:35.300 And if you're not, I just want to make sure we're bringing you along for the ride. So in the liver,

00:57:40.500 when you are taking C16 or C18, but let's just keep the discussion simple and start with a saturated

00:57:46.480 C16, the first committed step is going through SCD1 as an enzyme and it adds that double bond.

00:57:54.960 It makes a few more steps along the way, but ultimately it is increasing a process of lipogenesis.

00:58:01.240 It is making more lipid. It is increasing the amount of lipid within the cholesterol ester and

00:58:06.680 the triglyceride. It is being exported from the liver. So in response to your question, Sarah,

00:58:12.200 is this protective? I guess the answer looks like the body is saying, well, gosh, I would rather get

00:58:18.000 this fat out of the liver than keep it in the liver. And we know that it's not fully successful

00:58:22.500 in doing that because of course, although it hasn't come up yet on this discussion, everything we've

00:58:27.820 talked about today runs hand in hand with non-alcoholic fatty liver disease, which is truly

00:58:33.340 an epidemic at the moment. But I suspect that the body is still doing its best, even in the case of

00:58:39.560 non-alcoholic fatty liver disease, to try to export this fat as much as possible. The triglyceride is a

00:58:44.340 very efficient place to store it. I've always believed obesity is a protective mechanism. I think

00:58:52.580 that obesity is not the cause of metabolic illness, but the result of it, which is not to say that the

00:58:58.800 inflammatory environment that comes with it doesn't pour more gasoline on that fire. But it is my

00:59:05.560 belief that everything we're talking about here is the body's aim to protect itself from an abundance

00:59:11.960 of nutrition. And so that's how I read this is the body is doing, and specifically the liver,

00:59:18.280 which is arguably the most important organ in this situation, that the liver is really trying

00:59:22.400 to protect us. And it's saying, I'm making so much extra fat right now because you as my individual

00:59:29.660 are so far above your carbohydrate consumption tolerance, your tolerance for carbohydrate consumption.

00:59:35.200 And this is the most efficient thing I can do, which is turn that into fat, send it out via the VLDL,

00:59:42.160 get that into the adipose site. And yeah, you're going to be a little bit fatter and it's going to come

00:59:46.500 with some downstream problems, but in the short term, it's protecting me, the liver. Would you agree

00:59:52.000 with my teleologic view of that? I 100% would agree with it. And again, I think that we're going to

00:59:59.900 have more and more details on this coming out very soon in many research projects that are currently

01:00:06.720 ongoing. But what it really comes down to is we want to know what an individual's carbohydrate

01:00:14.500 tolerance is. Okay. I mean, that's key to personalization, right? Does everybody need to

01:00:22.600 be very low carbohydrate, low carbohydrate? I mean, where does, we can say population level,

01:00:29.500 what happens in large clinical trials, but what's happening with the individual? Because let's face it,

01:00:36.040 Peter, and you know, you and I as practicing clinicians know this, when you're sitting with

01:00:41.080 one patient in front of you, you can go over group data from a clinical trial. And that's important

01:00:48.040 part of the decision-making. But the only thing that really matters is what's going to happen with

01:00:54.560 the patient right in front of you. We really want to know what the individualized reaction is going to

01:01:01.680 be. We know that this happens with a carbohydrate consumption above a certain threshold. But what that

01:01:10.280 certain threshold is in the individual, we don't know. And based on these pathways, you know, what is the

01:01:17.680 marker we want to be looking at? Actually, it's probably POA, surprisingly not a fatty acid. But what this tells us

01:01:28.320 is that when someone has consumed carbohydrates above their individual tolerance, that POA level is going to be a

01:01:40.260 great biomarker. It's going to go up as, again, a protective mechanism in the liver. Our livers are

01:01:49.560 really, I mean, we talk about livers all the time, so related to insulin resistance. It's just always

01:01:55.320 amazing just how sophisticated and how our livers, although we think of them as producing things that

01:02:02.540 aren't necessarily good for us, and that may be true, they're also really working for us as well.

01:02:08.840 And so, again, I want to also go back on one other thing that you said. And the other thing that you said is, so this

01:02:17.320 comes before the adiposity. And I think that that is such an important point, and one, I like to preach every

01:02:25.980 opportunity I can get it. But this is starting to happen before people gain a lot of weight. Okay? This is a disease

01:02:35.880 process in and of itself that causes obesity. So we have to really take that into account when we're in

01:02:46.080 the office with someone who's struggling with obesity. And I know, Peter, you take this really

01:02:51.680 to heart, approaching and treating these patients without bias, as I do. But it's so important for

01:02:58.220 other providers to be looking themselves in the mirror and asking themselves, what are the biases

01:03:04.140 I hold against patients who come to me struggling with their weight? And what do I really know about

01:03:12.000 the science? And what it really, one must conclude is that this is not their fault. These are things that

01:03:20.140 happened beforehand, and they're suffering the consequences of it. And the problem is, the consequence

01:03:26.220 is on full view for everyone to see. It's not something that they can hide. And that makes them

01:03:33.400 so vulnerable to bias in healthcare. And again, one of the other things I come back to is part of our

01:03:40.060 whole battle in health equity. So Sarah, I want to keep digging into this idea, because it's so

01:03:45.880 interesting to me of having a leading indicator for this early, early, early warning sign. We talked about

01:03:54.260 it at the outset of this discussion, which is, in some ways, the tragedy of using hemoglobin A1c as

01:04:00.720 the marker of when somebody gets on the radar. I mean, you said it yourself, patients will show up

01:04:06.060 and nobody's ringing the bell until their hemoglobin A1c is above 6.5. But that literally is happening 10,

01:04:14.440 15, maybe 20 years after there were early, early molecular warning signs. And if measuring palmitoleic

01:04:22.660 acid is one of them, that's exactly the kind of stuff that I find interesting. Because in our

01:04:27.120 practice, we use CGM a lot. So continuous glucose monitoring, non-diabetics are wearing CGM like it's

01:04:33.780 no tomorrow in our practice because of that exact reason. We're basically holding them to a very high

01:04:38.720 standard of average glucose and high excursions and all these sorts of things.

01:04:42.520 I want to go back to something that you alluded to, which is the association between palmitoleic

01:04:48.360 acid and triglyceride is so tight that would we miss, for example, African-American patients? Do we

01:04:54.840 know if they're failing to synthesize C16-1 in the way a white patient is?

01:05:02.380 Wouldn't we love to know that? There's not been a good trial looking at that. I mean,

01:05:08.420 one of the problems that we have in research in general is that we tend to focus on white people

01:05:14.220 and actually worse middle or upper middle class white people. So there are a lot of questions with

01:05:21.220 this in specific populations. There have been a couple of studies recently coming out looking

01:05:28.580 specifically at what we're talking about POA and its marker for future problems and predictor of future

01:05:37.100 diabetes and other issues. One was a study recently published called the panic study, looking at levels

01:05:46.340 in childhood and seeing how they translate to health consequences, you know, decades down the road.

01:05:52.740 And then there was another study, I believe it was from the Netherlands, where they looked at POA levels

01:05:59.860 at 50 to correlate them with C-reactive protein levels at age 70, right? And what we see is what we

01:06:09.140 would expect based on our discussion here, which is the POA was a predictor of problems down the road

01:06:15.860 in people who were healthy when their POA was elevated or healthy. So we thought what we really

01:06:23.940 want to know ahead of time. And I know this is very meaningful to you and your practice is I want the

01:06:30.500 person who's healthy so I can get to tell them how to stay healthy. We've talked a lot about trying to

01:06:39.300 work on people who are already so, so to speak, behind the eight ball and we want to work them out and we

01:06:44.820 want to regress their disease, clearly an important goal. But we also really, if we're going to make

01:06:52.260 a difference, again, with the individual and population-wide, we need to know who's headed for

01:06:59.940 trouble. Again, I hope there's an ongoing effort here because I think this is the future of medicine,

01:07:05.220 right? I mean, I think the future of medicine has to be coming up with tools that allow us to take

01:07:12.580 broad sweeping population-based insights and very quickly target individuals. And if we have biomarkers

01:07:20.820 like this that can say, look, the moment this is triggered above a certain level, it doesn't really

01:07:26.020 matter what your glucose is and your insulin might still be normal. This is time to intervene. And then,

01:07:31.140 of course, the second part of that equation is what's the right intervention and how do we pair people

01:07:34.900 to the right intervention? Again, you and I have a very similar set of experiences, which is patients

01:07:41.540 with hyperinsulinemia and elevated glucose generally respond well to carbohydrate restriction. My practice

01:07:49.780 also focuses so much on the role of glucose disposal and non-insulin-dependent glucose disposal through

01:07:55.700 exercise. And I know that that's probably not a surprise to many people is sort of correcting the sleep,

01:08:01.620 exercise, nutrition, trifecta, and then adding to that the role of cortisol in all of this. So

01:08:08.180 I think this is a very hard problem to solve. That's the bad news. But I think the good news is

01:08:12.900 if you get this one right, you get a leg up on every chronic disease. So your risk of heart disease,

01:08:20.260 cancer, Alzheimer's disease all go down. And so it's worth this enormous effort to continue pushing on

01:08:28.020 these questions. On that note too, and when we talk about individualization and risk prediction before

01:08:34.900 we're seeing our classic biomarker issues come up, has to do, I'll circle it back to carbohydrate

01:08:42.260 restriction. Because we know very low levels of carbohydrate restriction can reverse the disease

01:08:49.540 process, bring about normal glycemia in patients and be able to get them off of medications. But we could

01:08:56.900 put a risk predictor like POA into wider use, okay, which would give a person their individual

01:09:04.020 carbohydrate threshold. What if it didn't need to be as low? What if we caught them earlier in the

01:09:10.660 disease process and we're like, hey, buddy, you go over, you know, 175, that's where trouble comes in.

01:09:17.860 Rather than you need to stay very low indefinitely because we've caught you on the spectrum of the

01:09:25.620 disease so late. And this is what we really need to do to control this, to keep your glucose normal

01:09:33.060 without the use of these many medications, especially insulin. I want to ask you another

01:09:39.460 question on this, Sarah. And again, I don't know if it applies to patients that you've treated with

01:09:44.260 diabetes or those in the pre-diabetes category, but have you treated patients for long enough on

01:09:51.460 ketogenic or very low carbohydrate diets who showed up in a state of metabolic disarray,

01:09:58.740 ran through a lengthy period of this. So maybe spent years on a carbohydrate restricted protocol

01:10:06.260 and everything gets better. So they, you know, the weight goes along for the ride, but obviously

01:10:10.900 and more importantly, their metabolic markers improve and they gradually reintroduce some amount

01:10:15.940 of carbohydrate back in the diet. And all of a sudden they're fine. Almost as though you reset

01:10:21.220 them during a long enough period. How often do you see that? And what do you think is the best

01:10:26.580 explanation for that? See it all the time. And the best explanation for it is what is their insulin

01:10:31.860 reserve? So the majority of people can go ahead, starting out even at long-standing diabetes,

01:10:40.340 reverse their disease, get normal glycemia, get off of all their medications, and then slowly

01:10:47.060 reintroduce carbohydrates as long as they have functioning beta cells. Okay. The problem is

01:10:54.740 the longer you've had diabetes clearly is a risk factor for this. And we can, we see evidence of that

01:11:00.900 in the bariatric surgery literature as well. I mean, there's been so many studies looking at

01:11:05.140 beta cells. And the fascinating thing is who is getting back some of their beta cell function. In

01:11:13.620 other words, maybe their beta cells were only dormant and were able to wake them up again,

01:11:19.860 versus which are gone and not coming back. I mean, the fact that people were on the incredibly

01:11:27.620 high dose of insulin, okay, starting on a very low carbohydrate diet. And then they got better right

01:11:37.540 away. A lot of the change is swift, but they couldn't get off insulin. And it was just years went

01:11:44.980 by, right? And they're just staying on this much lower level of insulin. And then all of a sudden,

01:11:51.780 they come off of it. I mean, logic would tell us that some sort of beta cell function has returned.

01:11:59.380 It took a long time. Reset the system, help them heal. You know, I mean, we don't completely

01:12:06.020 understand this. There's so many great scientists looking at this right now, but we still don't have

01:12:11.540 a certain answer, you know, because the answers on the personalized level is how many of mine are dormant?

01:12:17.140 How many of mine are dead, right? What's it going to take for me to wake these up? If it's impossible,

01:12:22.980 I'd like to know that because that sets expectations ahead of time, right? You can get a lot better,

01:12:28.980 but there's always going to be a little insulin in your life. It doesn't mean if they are someone who

01:12:35.220 doesn't have any insulin production capacity, that they can't get a lot healthier, but they may not

01:12:42.260 ever be able to get off of insulin. And so that's where it gets down once again into that nitty gritty

01:12:47.640 personalization aspect. And wouldn't that be nice to know? But I think that the answer to the larger

01:12:55.240 question is why is this happening that some people can start to eat carbohydrates, not anywhere near to

01:13:03.040 where they were, but they're able to put some back into their diets versus people who can't is beta cell

01:13:10.240 function. Something in there that you said is very important that I don't think historically has been

01:13:15.740 communicated well enough to patients, which is that insulin, while an amazing and important hormone is

01:13:20.820 not benign. And there's a big difference between taking a hundred units of insulin a day to achieve

01:13:25.940 normal glycemia and taking 20 units of insulin a day to achieve normal glycemia. And you'll take the

01:13:31.680 latter over the former all day, every day, non-negotiable. And some patients will say, well, gosh,

01:13:37.660 I'm still on insulin, this hasn't worked and not realizing, no, you've had a five-fold reduction

01:13:42.240 in your insulin requirement. That's an enormous improvement in your health outcome. And let's put

01:13:47.440 the economics aside. The economics are enormous, but ignore that for a moment. Just in terms of health

01:13:52.820 outcomes, the negative effects of hyperinsulinemia. I just want to say with that, you know, if we really

01:13:58.340 think about the way we manage diabetes rather than work to actually reverse the disease process and get

01:14:06.040 people off of medication, I mean, management constantly leads to more and more and more

01:14:12.360 insulin, which we know, I mean, on the outward, the appearance of it is that people gain more weight

01:14:18.280 when they go on more insulin. But, you know, if we really get down to the nuts and bolts, when we

01:14:23.780 take someone with type 2 diabetes, whose glucose is out of control to the point where we need to put

01:14:28.740 them on insulin, the mandatory discussion that needs to occur is, I'm going to give this medication,

01:14:35.600 this insulin that you're going to inject to you. And I'm going to do that because your blood sugars

01:14:40.760 are so high that they could acutely kill you, put you into the hospital, put you at risk of all these

01:14:48.140 complications. But I just want you to know you're more likely to die on insulin. That's what we need

01:14:55.340 to tell people. That's the truth. And, you know, that would have changed the approach a lot of

01:15:01.880 patients want to take. And it would certainly, if providers were forced to look at it that way,

01:15:08.020 when they're staring each individual person in the face, maybe they would treat it differently as well.

01:15:14.380 Yeah, I agree. So I want to talk about something that has been such a big part of your life in the

01:15:21.160 last few years. And people who don't know you may be almost surprised at where we're going in this

01:15:26.280 discussion now. But, you know, this discussion could basically continue down the path. If we

01:15:30.980 could talk more about diabetes, we could end this discussion here. And people would say, wow,

01:15:34.760 that's a really insightful, thoughtful person. But there's a whole other side to your experience

01:15:40.060 with healthcare, Sarah, that started, gosh, almost four years ago. I'll tell the beginning of the

01:15:44.740 story just from my end. So you and I obviously met each other through Virta, your early part of the

01:15:51.920 creation of this company, which is basically scaling up a way to remotely treat patients with type 2

01:15:59.000 diabetes. This is a company that Steve Finney is also a co-founder of, along with Jeff Olick,

01:16:04.020 I believe. I have a minimal involvement in that company. I'm a small investor and at one point was

01:16:09.940 an advisor. But it was during one of these advisory meetings that you and I happened to be sitting next

01:16:15.520 to each other. Now we'd met many times before that, but I do remember this very well. It was,

01:16:19.420 I think, June of 2017. It was up in San Francisco, a large U-shaped table in the room. And, you know,

01:16:27.040 it was a two-day ordeal and you were sitting to my left and that gave us more time than most times to

01:16:33.540 be chatting about this, that, and the other thing. And you looked in perfect health as always. And

01:16:38.300 at the end of the second day, I said goodbye and see you next time and blah, blah, blah, blah, blah.

01:16:43.720 And then about a month later, I heard from a mutual friend that you had been diagnosed with lung cancer

01:16:49.840 and I just about fell off my chair. So can you tell people what happened that summer,

01:16:56.280 the summer of 2017? Yeah. So I'll just start by saying I've been someone who's taken care of

01:17:03.840 themselves to the max all my life. Eating well. I've kept my weight at a normal weight. Even nine

01:17:12.680 months pregnant, I would have still been considered normal weight. Exercise like crazy. Competed in,

01:17:18.040 you know, half marathons, triathlons, Olympic distance. I did everything right. Never smoked,

01:17:25.160 never drank to excess. And it was June 30th. So right after that, it was June 30th of 2017. I was

01:17:34.780 having a normal day. I was, went to exercise. I had a big IRB meeting in the morning, went home due to

01:17:43.420 my wonderfully full house of three kids and took a business call in the basement. Cause that's was,

01:17:50.700 that's always my escape place where it can be a little less noisy. And all of a sudden I couldn't

01:17:56.280 talk and I, I couldn't figure out what was going on. I knew something wasn't right, but I couldn't

01:18:02.440 speak. And all I know is that I hung up the phone at some point cause I was embarrassed. I was,

01:18:09.580 remember thinking there, he's going to think I'm drunk. The next thing I remember was being in the

01:18:17.540 car with my husband and him saying, I don't think we could take you to urgent care. I have just very

01:18:23.280 flashes of this day. And the next memory is in the trauma bay at the hospital, the hospital that I

01:18:31.880 work at where I had seen patients many, many times. And I'll have to tell you the other thing is the

01:18:39.100 last time I had been in that particular trauma bay was when I brought my then four-year-old daughter

01:18:44.860 in or my husband did. I met them via an ambulance after a traumatic brain injury. So it was like a

01:18:52.740 very bad place for me, although my daughter completely recovered. And I remember screaming

01:19:00.580 at my husband that they're wrong, they're wrong. And I wanted to see the computer because what had

01:19:07.360 happened when they first came in as they thought it was a stroke. And so my poor husband was all of a

01:19:12.720 sudden tasked with, you know, are you going to give her clot busting medication or not? Because we

01:19:18.760 think she's having a stroke. But lo and behold, the imaging showed a really large tumor in my brain.

01:19:26.240 Then they imaged the rest of me and it turns out I had multiple tumors in my chest. And so they

01:19:34.240 presumed, you know, correctly at that point that this was lung cancer, but I also needed emergency brain

01:19:40.580 surgery. I remember most of this by people telling me about it. So anyway, the next day I had a

01:19:49.380 urgent brain surgery. And then being a physician in lung cancer, you know, I was like, that can't

01:19:56.840 possibly be, you know, I have never smoked. You know, how do I have lung cancer? I am the healthiest

01:20:02.160 person I know. I remember being in the hospital because of course, you know, you're on drugs and

01:20:07.040 everything else and shock and everything. And I kept saying, look at my nails. These are the

01:20:12.140 healthiest nails you've ever seen. How can this be a person who's sick? Because somehow that was like

01:20:17.000 just one example of how that's impossible. Talk about the stages of grief and denial, right?

01:20:24.360 And being a physician and knowing what lung cancer meant, the next thing that came out of my mouth is I

01:20:29.600 want to move to Oregon because I was like, I know what this means for me and I know what this means for

01:20:34.340 my family. And I don't want to play any part in this. I don't want them suffering. Can you tell

01:20:39.460 folks what you mean by that? Not everybody might understand the implication of what you're saying.

01:20:43.300 I wanted to go to Oregon because they had physician assisted suicide. Because I, you know,

01:20:49.640 I knew I have treated so many patients with lung cancer. I knew the horrible end. I knew what this

01:20:57.400 meant. The suffering. Especially when it spread. Yeah. And it had spread everywhere. I mean,

01:21:03.580 I had stage four lung cancer. You know, the day before I had been fine, a hundred percent fine.

01:21:10.380 That morning I had exercised vigorously. And suddenly I'm in the hospital recovering from a

01:21:19.500 brain surgery, being told that I have a rapidly fatal disease. And, you know, all you can think of

01:21:28.420 in that moment of panic is your family, right? And so, you know, my only thought was I don't want

01:21:33.840 them to watch me go. I want them to remember mom. And so, I mean, there began my so far almost four

01:21:44.480 year journey of a new me, you know, cancer changes you. So I'm not that person. One of the many things is

01:21:55.480 sometimes at this point in time, you know, I mourn that person. Cause I really, I liked her.

01:22:05.920 I mean, one of the things that I think is very shocking for people to understand is that

01:22:12.720 it's probably between 12 to 14% of people who get lung cancer are not smokers. And they all tend to

01:22:20.800 get a certain type of lung cancer. You know, lung cancer is broadly divided histologically by small

01:22:26.520 cell and large cell or non-small cell, I'm sorry. And within the non-small cell, there's large cell,

01:22:32.040 adenocarcinoma, squamous cell. And most of the people like you who are not smokers get this type

01:22:37.780 of adenocarcinoma, non-small cell. And it is really shocking to think that given the prevalence of lung

01:22:44.720 cancer and the lethality of lung cancer, lung cancer kills more people than any other cancer.

01:22:51.080 And I believe that's true for male and female still. Yes. I mean, by far.

01:22:55.800 Yeah. To think that such a high percentage, 12 to 14% could be non-smokers tells us this,

01:23:01.920 the severity of this. I also think it's worth reiterating something you've said,

01:23:07.020 which is sort of the miracle of the fact that we're sitting here having this discussion four years

01:23:10.760 later. The median survival, meaning if you took a hundred people with stage four, which means a type

01:23:21.020 of cancer that has spread from its original site of origin. And in your case, it went to your brain,

01:23:25.400 which is a particularly devastating place for this cancer to grow. The median survival of people

01:23:30.360 with stage four lung cancer is probably 12 months or less, correct?

01:23:35.360 Well, it depends on what kind of lung cancer that you have. And sometimes even eight months or less.

01:23:43.940 Those were the stats that I knew when I was first diagnosed. And one of the things that I'll say is

01:23:52.980 non-smoking lung cancer is growing at scary rates. It's being diagnosed and it hits people

01:24:02.020 in their prime. It's growing rapidly, especially in young women. So it's hitting a lot of moms. 0.98

01:24:10.340 Much more common in women than it is in men, although it does happen in men. Happens in Caucasian 1.00

01:24:17.200 and Asian women predominantly. And the interesting thing is most of the people that it impacts are thin

01:24:23.500 and in shape or athletes. So it goes against everything.

01:24:29.820 Do we have any insight into why?

01:24:33.320 No. And it's one of the things that's not being investigated as much. When you look at,

01:24:40.020 okay, what studies have been out there? Oh, we get the typical, it's radon. It's being next to a

01:24:45.760 smoker. I never was. Okay. My father was a smoker. He quit smoking the day I was born and never went

01:24:51.300 back. I was not raised around smoke. So the fact of who it's impacting and the fact that the demographics

01:25:02.140 of the people that it's impacting are the healthy people, unlike what we associate with our epidemic

01:25:11.300 of insulin resistance, that's not who these people are. We know that insulin resistance is responsible

01:25:17.240 for a huge number of cancers and cancer rises. That's not this. It's young women. And again, 1.00

01:25:26.720 who have presumably done everything right. And it's just, it's something that is not getting enough

01:25:33.660 press. I know the Guardian did a big story about it about a year ago, but otherwise it's not getting

01:25:40.320 the attention it deserves. And these women really wind up with two different kinds of cancer. They 1.00

01:25:47.020 wind up with EGFR driven cancer. That's epidermal growth factor receptor, or they wind up with something

01:25:55.360 called ALK positive cancer. I have the EGFR, specifically something called EGFR exon 19 mutation.

01:26:05.920 And the thing I didn't know at diagnosis, because again, I had been focused on obesity and metabolic

01:26:14.140 disease and diabetes for so long, I hadn't been seeing as many people with active cancer as I did

01:26:21.880 when I was in primary care. And so I was quite frankly behind on some of the newer treatments and newer

01:26:32.180 diagnoses, if you will, and we're talking the genomics of cancer. But for EGFR cancer, there was

01:26:41.760 something called a targeted therapy. This class of medications is called tyrosine kinase inhibitors,

01:26:49.520 and people can go on them and they can get better. Okay. They can even in many cases have all of the

01:26:58.460 cancer go away. It doesn't mean they're cured though, because it always comes back. And so after

01:27:06.300 initially, again, going through all these, I mean, I'll tell you the denial grief stage.

01:27:13.800 I want to actually ask you exactly about that, Sarah. I want to go back to what is it like when

01:27:19.380 you were recovering in the hospital from the brain surgery? Because I assume they had not taken out the

01:27:24.180 primary tumors in your lungs. They were just alleviating the most life-threatening symptom

01:27:29.580 you had at the moment, which was a mass inside a part of your body that can't accommodate a mass,

01:27:34.520 which is why you had a seizure. So they take that out. You're recovering from a surgery that by itself

01:27:40.280 is difficult to recover from, but then coupled with the knowledge of here's this disease and

01:27:46.180 my lungs are full of this. What do you remember of those days?

01:27:52.900 Overwhelming grief to the point of not being able to think, you know, of course I come and approach

01:27:59.020 everything in life as a mother. And I'm not saying as a mother only, like fathers would do the same

01:28:04.900 thing, but you approach every problem in life through what it means for your children.

01:28:12.020 How old were your children at the time, Sarah?

01:28:15.000 They were 7, 12, and 14. And they needed me. They still need me. And so the grief is overwhelming

01:28:27.020 about what I quickly realized is I'm going to break my children's heart and there's not a thing I can do

01:28:36.600 about it. And to have that realization because it comes quick and have to sit with that

01:28:44.820 is a grief I can't, I can't even explain. And so initially I just was, I couldn't handle the grief.

01:29:00.420 I had to be denial, in denial. I came home from the hospital. I had just been discharged from ICU

01:29:08.200 and I walked seven miles the day I got home. And my feeling was, see, I can't be sick.

01:29:16.000 I just got out of the brain surgery. I'm still on medication. I walked seven miles today.

01:29:21.600 I'm healthy. I don't know what you people are talking about.

01:29:24.820 What did your kids know at this time? Had your husband already spoken with them?

01:29:28.800 Well, sadly enough, and I actually didn't find this out until quite a bit later. They are the

01:29:34.380 ones who found me in the basement. So, you know, talk about not telling the children. That was never

01:29:43.120 an option for us. So they knew I was having surgery, that there was a tumor in my brain and that this was

01:29:54.300 cancer. This is not good. And that's a lot for a kid to unpack, right? Especially a kid, you know,

01:30:06.900 again, it's hard for any kid to unpack. But, you know, one of the things I remember when my kids

01:30:11.920 were going through each of their own, everyone, kid goes through at the phase of, what if something

01:30:17.180 happens to you, mommy? What if something happens to you, daddy? Right? All kids go through that.

01:30:22.000 And the one thing we used to kind of laugh together, my husband and I, about that.

01:30:27.520 Say, oh, honey, your mommy and daddy are the healthiest people. We are so healthy. You don't

01:30:35.100 need to worry about that. And I remember that. You know, it's one of the first things that you

01:30:40.020 think of when you're put in this situation is, oh, my God. You know, they have to unpack this

01:30:46.780 in that context. And it's hard to be a teen. It's hard to be a seven-year-old. But to be one

01:30:56.620 whose mother suddenly had a, you know, diagnosis of advanced cancer. And we, it was a hard decision

01:31:07.060 on what to do, but, you know, in talking and how do we handle the kids. But the one thing we decided

01:31:12.280 together, I mean, my husband and I, is that we were never going to lie to them. We were

01:31:19.180 always going to tell them the truth. Because I thought that the worst thing for a kid is

01:31:23.560 to constantly be wondering if something, if there's going to be a huge shoe that drops.

01:31:28.820 And so we told them, we tried to open up the lines of communication. They mostly didn't want

01:31:36.560 to talk about it. But we told them that we were making that promise to them. And we have never,

01:31:42.420 never gone back on that problem and promise and never will. I mean, that's one that it's really

01:31:48.140 important to me. We may delay telling them something for a little bit until we really know the facts. But

01:31:55.020 as soon as we really know the facts, they're going to hear about it. And over time, in grief,

01:32:03.400 you learn to accept many things. My husband and I, our dream had been to retire to a farm and make

01:32:13.980 gourmet butter. Like that's what we were going to do. That was going to be the second career, right?

01:32:19.380 And you learn to make peace with that's not the case anymore. You know, we always used to joke that

01:32:26.060 the way we wanted to die was 95 years old on the way home from a skiing trip in a fiery car accident

01:32:35.160 where our kids would not have to deal with the bodies. But we wanted to make sure it was on the

01:32:40.220 way home. The cremation, the two for one. A two for it was going to be on the way home because we were

01:32:46.680 going to be having fun up until that point. So that's acceptance. You know, you're not going to

01:32:53.020 retire. You're not going to have all these things, but you can't accept that you're not going to be a 0.94

01:33:00.460 mom. Impossible. Now, at some point, I'm guessing kind of the problem solver in you started saying

01:33:08.260 like, hey, I'm going to learn as much as can be known about this. And we're going to talk about

01:33:15.240 this in the context of the asymmetry that exists. I just had a discussion about this with,

01:33:21.200 we have a weekly meeting in our practice with all the providers. And, you know, we just had this

01:33:27.160 weird situation recently where, you know, basically a patient of ours who has another physician

01:33:33.780 was kind of caught in the middle of a recommendation that turned out not to be the

01:33:38.420 right recommendation. And, you know, we were able to get them a referral to somebody else who basically

01:33:43.480 got them out of a very unnecessary surgery. And we were just sort of thinking, man, like,

01:33:50.100 we're so glad that that patient was able to dodge that bullet. You know, they were going to have

01:33:53.880 a surgery that they totally didn't need. That's a very big surgery with lots of risks. And we realized

01:34:01.660 like the asymmetry of knowledge in medicine is so overwhelming that it is, it's not even just about

01:34:10.060 money or education outside of medicine. Like a smart person still has a hard time digesting medical

01:34:17.440 literature. And like I said, we're going to talk about this, but, you know, you very quickly must

01:34:22.720 have figured out, Hey, I have this EGFR 19 deletion. So we no longer talk about this as you have lung

01:34:30.640 cancer or you have adeno, or you have non-small cell. We're really going to refer to it by its

01:34:35.940 mutation and everything will come down to how do we treat that? How long was that process for you to

01:34:42.040 say, I'm going to, I don't know if this is the right word, but I'm going to partition my grief

01:34:47.660 and my problem solving brains. And I'll do both of them, but I'll, I'll move back and forth.

01:34:54.820 It happened pretty quick, which is, okay, this is terminal, right? You have to come to grasp at that,

01:35:02.720 but terminal when, and what can I do to control the when?

01:35:10.600 But when you say that, Sarah, did you really come to that realization so soon? Because

01:35:14.760 technically life is terminal. I mean, there's nobody listening to this podcast, watching this video

01:35:21.280 who isn't going to die. So that's all terminal. But when you say that, do you mean that immediately

01:35:28.280 and without question or reservation, you felt that you would not live a normal life expectancy? There

01:35:33.940 was no hail Mary out there that was going to take you to being the 95 year old skier?

01:35:40.680 Yeah. I mean, I, I think just the reading and understanding, although the advances that this

01:35:47.080 was going to be terminal really soon, you know, in my life. And I was only 46 at the time. And,

01:35:55.880 you know, my first thing was just, please let me make it to 50. I'm 49.

01:36:02.440 You're going to be 50 soon.

01:36:04.240 Yeah. I'm going to be 50 in the not too distant future. So, you know, that was like, my first one

01:36:09.560 was just like, okay, let's, but right from the beginning, I'll tell you the when was 11 years.

01:36:17.040 Okay. And that has not left. I don't need to be 95. I can accept all those things that I'm going to

01:36:24.640 miss out on by not growing old. I just need 11 years, which to everyone was unrealistic,

01:36:33.000 but why 11 years? Because my youngest would be graduated. So immediately my goal was,

01:36:43.040 I can't settle for less than 11 years. I have to make it to 11 years. And so in became that,

01:36:51.020 like my war cry, 11 years, 11 years, I have to make it 11 years. And that started me on a path of,

01:36:59.380 oh my gosh, so much. So the first thing I thought in reading all the, I mean, read everything is I

01:37:05.060 got to get this primary tumor out. You know, I'm considered inoperable, but we know that having this

01:37:11.140 primary tumor here increases my risk for mutations. Okay. Remember I said that the tyrosine

01:37:16.640 kinase inhibitors or the TKIs, they work amazingly well, but only so long, you know, somewhere between

01:37:25.240 eight and say, you know, on average eight and with the more advanced ones at the long end is like 24 to

01:37:35.780 30 months. Okay. So that's not enough time. That doesn't get me to 11. So I was like, okay, you know,

01:37:44.100 this is increasing the risk for mutation, which is how these develop resistance to the tyrosine

01:37:50.300 kinase inhibitors. And remind me, Sarah, you, because I remember you emailing me probably by

01:37:56.060 August and starting to explain some of the details. Your biggest tumor was like five centimeters. That's

01:38:03.780 a monster tumor. How many tumors did you have? It was six centimeters or you had six tumors?

01:38:09.100 It was six centimeters, which is amazing in the sense that I never had pain from it. I never had a

01:38:17.240 cough. Probably because you were so healthy. I think so. Because talk about being caught out of

01:38:22.620 the blue. You know, there just wasn't this premonition of something is awry and I'm just

01:38:27.600 not addressing it. So the standard of care was just that we typically don't operate on patients with

01:38:34.380 metastatic tumors. The only reason they operated on your brain was it was an acute way to save your

01:38:40.460 life. I think it's hard for patients listening to this to understand that, but that's the playbook

01:38:45.660 in oncology, right? When a patient shows up with metastatic cancer, they're considered not surgical

01:38:51.460 candidates. And this was the exception and not the rule. You were going to be dead probably within days

01:38:57.100 if they didn't operate on your brain. But all this time afterwards, you still have this burden

01:39:03.200 of tumors in your lung. And now the question is, can we improve your prognosis? And maybe that doesn't

01:39:10.600 mean you live to 95, but can we reduce, can we make your cancer less resistant to therapy by taking

01:39:18.900 the majority of the cancer cells out of your body?

01:39:21.280 Right. And decreasing the tumor burden because really quickly the TKI got rid of every single

01:39:28.720 small tumor. I had them throughout, you know, like paint splatters on throughout both lungs

01:39:34.740 and they were gone in a matter of weeks.

01:39:37.960 That's staggering, isn't it?

01:39:39.540 I mean, it is. It's remarkable. But, you know, again, the primary tumor was huge. So I had,

01:39:46.360 unfortunately, the large tumor in my brain was not the only one. I had two other ones that they

01:39:52.520 radiated. They didn't need to be surgically removed. They were small. They could be radiated.

01:39:57.380 And then I set about trying to find someone who would take out this primary tumor.

01:40:03.320 Can I ask you about the stereotactic radiation, Sarah? That's, I mean, we glossed over that,

01:40:07.940 but that's not a benign process either. Did you suffer nausea from that? How difficult was your

01:40:14.220 stereotactic treatment? Did you take it all in stride?

01:40:17.520 I did great with the treatment to the brain. I didn't have any issues. You know, I did have

01:40:24.560 issues at the beginning, but they were more to the TKI. You know, one of the things with every

01:40:29.780 specialist that I saw, they couldn't believe it or they told me if I saw them earlier, it wasn't

01:40:35.940 going to happen. You know, at least you'll keep your hair. All my hair fell out. Like it wasn't

01:40:41.140 supposed to happen. Like your hair is not supposed to fall out with TKIs. All my hair fell out.

01:40:46.760 Anyway, so the brain radiation went fine. And then I met a surgeon who was going to take out

01:40:53.380 the primary tumor for the reasons that I was saying. We just, anything to decrease the risk of

01:40:59.560 developing a mutation that keeps me from being sensitive to the TKIs. And so I went in for surgery

01:41:08.540 in September. And I can remember her saying, we're going to take this tumor out. We're going

01:41:15.000 to take out your right upper lobe. Unless of course, we've seen that there's disease in the

01:41:20.620 mediastinum. But there was no disease on the PET scan in the mediastinum. So she was feeling pretty

01:41:26.860 positive about being able to take that out. But I knew for several weeks beforehand that that was a

01:41:34.740 possibility. And just so folks know what we're saying, on the right-hand side, you've got these

01:41:40.100 three lobes here. But they drain into these lymph nodes that are in this middle structure called the

01:41:48.320 mediastinum. And so you had this monster tumor that was going to require the entire upper right lobe to

01:41:55.220 be taken out. But if the surgeon felt that on visual inspection at least, or maybe even sampling nodes,

01:42:02.400 that any of those nodes had cancer, it was her opinion that this is really futile. Because now

01:42:08.460 we know it's already escaped the lung. It doesn't matter. So you went into that surgery knowing you

01:42:14.140 could wake up with a huge scar in your chest, chest tubes coming out, and the cancer is still in you,

01:42:21.200 right? And that happened. And that was, it was terrible. I kept apparently under the influence,

01:42:29.700 I mean, everyone told me. I was so hysterical, screaming in the recovery room, I'm a mom.

01:42:37.840 You can't let this happen to me. I'm a mom. That's all I kept saying. And I, of course,

01:42:41.420 don't remember any of this, but they had to actually take me away, put me in a private room.

01:42:46.440 And that was all that I kept saying. So, you know, I had to come home and learn to accept that.

01:42:54.000 I now was bald. And I definitely fell into a deep depression. But at the same time,

01:43:03.960 I refused to completely give up. I mean, like, for example, I went back to work at the clinic the

01:43:10.140 same month that I had brain surgery, which sounds crazy. But this is part of this whole process. And

01:43:18.060 then, but after the surgery failure, that was terrible. And then I didn't really recover back

01:43:25.300 into my determined place until a really very specific moment. And that was just a couple of

01:43:34.320 weeks before my diagnosis. I had been selected to be an Aspen Health Innovator Fellow, which was,

01:43:41.920 I mean, this is among the highest honors for your work. The Aspen Institute is a place that brings

01:43:49.360 together thinkers in all kinds of disciplines. And to be chosen to represent people who are innovating

01:43:56.520 in the healthcare space was such an honor. And in order to do that, you had to commit to

01:44:04.220 four weeks of leadership sessions in the next two years, which, of course, at the time, I was like,

01:44:11.560 of course, sign me up. But as that first session inched closer, it was in November, I was so,

01:44:19.840 what do I do? I couldn't make up my mind. I literally didn't make up my mind for sure

01:44:25.380 until I sat, I got on the airplane. Because I was ready to run back. Because it was like,

01:44:32.480 I'm going to leave my kids for almost a week. I have terminal cancer. And at that point, I decided,

01:44:40.160 you can live feeling sorry for yourself. And of all the things that you're going to lose,

01:44:46.380 or you can go out and live. And your kids are going to be better for it. This is what really

01:44:54.140 made me decide. Your kids are going to be better if you choose to live. And so that was the moment,

01:45:00.580 sitting on that plane seat, crying. I've cried on a lot of planes since this diagnosis.

01:45:06.560 Deciding, I just chose to live. This was a moment. I made my choice. Now I got to stick with it.

01:45:15.180 And that's how I've tried to live my life since then. Because I have a platform. I had a platform.

01:45:23.780 I had done what I feel was a lot of good for a lot of people. And it wasn't finished.

01:45:32.760 And I knew that this was good for my children. And I'll tell you, one of the most impactful moments

01:45:39.280 of my whole life happened before my diagnosis. And it was one of these times where we were at the

01:45:47.700 dinner table and the lottery happened to be one of those, you know, hyperinflated lotteries. Oh my

01:45:54.040 God, you can win, you know, bajillion dollars. And so my husband and I were at the dinner table

01:45:59.680 joking around about it. Right? I mean, we don't play the lottery, but we were joking around,

01:46:03.820 maybe we should buy tickets. You know, we could retire. We could retire. And here at the time was

01:46:08.780 my 13-year-old son at the dinner table. And he got really upset about us discussing this.

01:46:16.880 You can't retire, Mom. You're doing so much good for the world. How could you even think of it?

01:46:24.560 I've never been so... That is a defining moment of my life. And like, I was like, oh my God.

01:46:33.460 You know, at the time, I just, I was so taken aback by that. Certainly that weighed heavily on my

01:46:41.760 decision to get on that plane and to continue doing what I'm doing. And what I'm doing has morphed

01:46:49.760 since my cancer diagnosis into an even greater focus on health equity because of my experience

01:46:57.580 as a cancer patient and someone who is privileged. Because I'll tell you, you have a much greater

01:47:07.780 chance of surviving cancer if you are, uh, has privilege. You know, one of the lucky ones. And I didn't

01:47:20.220 realize the stark differences until I became a patient. I want to talk about that in some detail,

01:47:30.480 Sarah, but I want to also understand how it is that we're still talking today, frankly. In other words,

01:47:38.220 how have you managed to stay in an equilibrium with this disease, right? I've always, I mean,

01:47:46.600 let me, let me share with you a couple of things that I, I've always struggled with when thinking

01:47:51.560 about cancer. I, I'm not fond of the language that we sometimes use around cancer and that we

01:47:59.000 beat cancer and that we can't give up and things like that. Because it almost suggests that the

01:48:05.580 patients who don't survive cancer have somehow given up. And I just, I, I just don't find that

01:48:10.460 in my experience, having taken care of many patients with cancer to be true. I think,

01:48:14.460 you know, it doesn't make sense to me. And I think the way that you said it and described

01:48:19.460 it earlier makes the most sense, which is basically finding a way to coexist with your cancer for as

01:48:25.280 long as possible. And you've exceeded all odds. I want to kind of understand that journey a little

01:48:32.460 bit more. It's one thing to go through the tyrosine kinase inhibitor, have this immediate response

01:48:38.960 that's remarkable, but then get this setback three months later where your primary is not only still

01:48:45.780 there, but you actually realize now there's, there's mediastinal involvement, which basically

01:48:50.620 means there's no question you have cancer cells elsewhere in your body. It's not like they stop

01:48:55.940 when they get to the lymph nodes. So pick the story up for us in terms of what your ongoing treatment

01:49:02.460 has been life. Like how have you stayed in this, in this state of equilibrium, so to speak?

01:49:08.740 So I haven't. Okay. On many occasions, I haven't. So after the surgery, the next thing that happened

01:49:17.820 is they found another brain tumor. There's argument as to whether it was there from the get-go or

01:49:25.020 whether it was something new, but either way they decided it would be considered that the first line

01:49:34.520 TKI that they had put me on had failed me. And so I got switched to, I got more radiation to the brain

01:49:43.040 and I was switched to the newest TKI, happens to be called osimertinib or chagriso. I was put on that

01:49:53.340 in November, right before I went off for my first Aspen Leadership Conference. And I had decided that

01:50:03.820 I do not accept being a sitting duck because what the cancer world then wants is for a patient like me

01:50:16.140 to just sit and wait for the cancer to come back, right? That's what you're doing. You know,

01:50:21.500 it's coming back. There's no question about it. And you know, it's coming back soon and you are just

01:50:28.860 waiting. And I couldn't accept that as a mother. I think I could accept it as a human, but I couldn't

01:50:35.200 accept it as a mother. And so I went on a journey to find someone who could treat me

01:50:44.140 in the most aggressive way possible who shared my view that sitting around and waiting for this to

01:50:53.960 come back was totally unacceptable. I traveled the country. I saw everybody. Let me tell you. First

01:51:02.740 of all, of course, that shows I have means to do that, right? That a lot of other people don't.

01:51:06.920 And I actually, along the way, met another mother, physician, my age, just a bit younger,

01:51:17.540 younger kids, who had the same attitude towards it. I refused to accept this. We sort of became a team,

01:51:24.660 so to speak, and wound up by complete serendipity meeting a group of physicians

01:51:32.560 physicians who really felt that the way to treat this long term was to be constantly battling it

01:51:42.020 with something new. So in other words, the cancer dogma right now is you put people on something at

01:51:49.680 the highest dose possible and you keep going until it doesn't work anymore. That's how we deal with

01:51:56.640 cancer. And then we switch and it's the same thing over again. And the idea is what if we hit it with

01:52:04.360 less and then change it up all the time, right? And this goes to the idea of beating the mutations

01:52:11.940 before they can get you. So thankfully, I had a physician here at home who was willing to say,

01:52:22.780 okay, that is worth a shot. February 2019, okay, because it took a long time to get to this point,

01:52:31.000 right, of searching, trying to find something. I started chemo, regular chemo. I went through the

01:52:38.660 regular cycles of chemo. And then when I was done with that, I immediately went to anti-estrogen therapy,

01:52:47.820 okay, because I had a very specific mutation besides the EGFR-1 and there was a medication to treat it.

01:52:58.460 It just so happened to be a breast cancer medication, but it was the same mutation for either cancer.

01:53:05.880 So immediately upon stopping the chemo, I went on the anti-estrogen therapy. So I was put into early

01:53:16.640 menopause with a number of regular medications, Lupron, Fulvastrant. And then I was started on a

01:53:23.500 medication called Pablacyclib, okay, which again is primarily a breast cancer medication, but was

01:53:29.840 targeting one of my very specific secondary mutations. I was on that for the summer and all this time I'm

01:53:36.900 still on the Tigriso or Asimertinib. That never stopped. As soon as the eight weeks of that was over

01:53:43.280 with, I went back on chemo, but very different. Low dose chemo. Single agent, very low dose.

01:53:53.520 So the first one was Cisplatin. And, you know, everyone says, oh, Cisplatin, you know, you're

01:53:59.500 going to do terrible on this. I mean, this is harsh. And it is. But, you know, I did fine. I mean,

01:54:05.880 I'm not saying I wasn't tired. I've basically been nauseous for the last almost four years,

01:54:12.160 every single day. You know, it's just you learn to manage that. So I learned to manage it. I learned

01:54:17.400 to manage, you know, being tired and the things that came along. I still traveled for work. I was

01:54:23.260 still able to do everything. I just, I could tell you some really crazy stories of things I had to do

01:54:30.060 while traveling to accommodate how I was feeling that nobody knew about at the time. But anyway,

01:54:36.880 some really wacky stuff that you do, but you just, you manage, you, you figure it out, right? You

01:54:42.120 improvise lots of improvising. And then I got switched to another after eight weeks, got switched

01:54:49.580 to gemcitabine or gems are. Which again, these are so crazy. You just don't think of this because

01:54:55.620 that's a drug that's typically used in pancreatic cancer, right? Well, yeah. And it can be used in

01:55:01.060 lung cancer too. I mean, it just depends on the mutation. I think that's the point, right?

01:55:04.800 Right. Yeah. Believe it or not, there's no standard chemo for lung cancer.

01:55:09.580 Can you believe that? There's not a standard, like standard of care regimen. So the thing is,

01:55:14.400 I wasn't doing any outlandish things here. Okay. These are all treatments for lung cancer. Like you

01:55:21.220 said, gems are, is used more for other things, but this is not an outlandish thing that's never heard

01:55:27.520 of for lung cancer. I mean, same with cisplatin. I mean, none of these things are, you know, I was,

01:55:33.560 oh my goodness, we're going to, you know, do something, you know, that's never, ever been

01:55:37.580 done before, you know, so to speak things. And at this point, which is now the fall of 2019,

01:55:45.260 where, if you go and get a PET scan, where do you actually have tumor in your body at this point?

01:55:51.480 So yeah, let me back up for a second because, well, the quick answer is I had no tumor.

01:55:56.960 There was no tumor anywhere. And to back up is that the TGRISO, this is pre-chemo,

01:56:06.400 had stopped shrinking my primary tumor in March of 2018. So this was, you know, almost a year before

01:56:16.600 I began chemo. And so since they wouldn't surgically operate it to get it out, I had it radiated.

01:56:25.340 Again, I was lucky enough to have a radiation oncologist who worked with me. And like I said,

01:56:33.300 I tolerated brain chemo well. The same was not the case to the lung. I had real issues. And

01:56:43.800 interestingly enough, we were leaving for, to hike the Inca Trail in May of that year. So I had had

01:56:53.060 radiation that we were leaving to hike the Inca Trail. And I started having kind of bad chest pain

01:56:57.240 like a day or two before we hiked the Inca Trail. I was like, okay, I'm sure this is just reflux. I'm

01:57:03.360 going to take some reflux medication. And then I was like, look, okay, if it's not, if it's more,

01:57:09.140 you know, what a better place to die than surrounded by your family on the Inca Trail and all the beauties

01:57:15.340 of the Andes Mountains. Okay. I can accept this. Let's go. You know, I didn't even tell anyone.

01:57:19.820 I was like going forward and did that successfully. It was great. My eight-year-old toodling along,

01:57:27.460 you know, she was always the fastest of any of us. We went with our friends and I mean,

01:57:32.000 amazing experience. I just have to say that those things, especially if you can get kids in it,

01:57:37.720 I'll never forget that when we all got back and we went and checked into the JW because we were like,

01:57:44.220 give me a shower, a very clean bed and a spa. My middle child, my daughter said to all of the adults,

01:57:53.900 I developed my third eye during that. It was one of those experiences. Like you don't normally think

01:58:01.220 you're going to get that out of a, you know, she was what, 14 at the time. We were all like, what?

01:58:09.300 But anyway, so it was a super special time. I was still having pain. And then my rest of my family

01:58:15.320 flew home. I actually had to fly from Lisbon to Switzerland because I had a conference I had to go to.

01:58:23.040 And at that conference, things started to get really bad. I made it through, but not with,

01:58:30.120 again, some funny stories of how I accommodated to it because I was having crushing pain.

01:58:37.760 Got home. Turns out, of course, I had some rare, I had this rare complication where it actually

01:58:42.700 impacted my bones. My radiation oncologist said, the only treatment for this is to put you on long-term

01:58:49.800 opioid therapy. And I was like, oh, no thanks. I will accommodate. There was no way I was doing that.

01:58:56.420 So I had to get through that, which was a, which that was a little bit of a saga. But anyway,

01:59:03.700 I had no disease then after that radiation, none. And so I was in this state, they call it

01:59:09.760 NED, no evidence of disease. I like to always say NED, right? I was NED for a really long time. I had no

01:59:17.080 evidence of disease. It was a great place to be, right? Still on treatment, still trying to do

01:59:21.700 everything to keep this from coming back and started GEMSAR. And, you know, everybody had said

01:59:27.700 all these terrible things about cisplatin and GEMSAR was 10 times worse. Everyone was like,

01:59:33.460 you'll be a breeze. GEMSAR is a breeze compared to cisplatin. 1.00

01:59:37.520 You are really the exact opposite of everybody because, yeah, I mean, we used to tell patients

01:59:42.120 GEMSAR is, it's non-chemo.

01:59:44.600 Yeah. Everybody tolerates GEMSAR. I can still remember sitting because I was feeling too crappy

01:59:50.380 to drive, my mother driving to pick me up to take me to chemo one day, sitting on my front porch and

01:59:56.300 throwing up in a plant on the way to chemo. There are nutrients in there, Sarah, that are very good

02:00:01.480 for the plant. So I wouldn't feel bad about that. That's very, it's a very healthy part of the carbon

02:00:06.160 cycle, I'm sure. But I was determined to keep on. I was really close to getting switched to taxols,

02:00:12.280 which, you know, I'm like, this is going to happen, that'll be better.

02:00:16.020 So then had to take another trip for another meeting and had lots of friends there. And I can

02:00:24.980 remember them standing behind me after we had eaten and they were pushing me up this hill in San

02:00:32.420 Francisco because I literally couldn't walk. And I kept thinking to myself, I'm a hypochondriac.

02:00:38.300 This is just because I'm anemic, whatever. I was super short of breath, but I'm like, okay.

02:00:45.940 I had convinced myself I was making it all up in my mind. I fly back from that trip and the very next

02:00:52.280 morning head in for chemo. And they immediately said, oh my God, no chemo. Everything is a mess.

02:01:00.800 My liver numbers were through the roof. My kidney numbers were high. I had pancytopenia so bad

02:01:08.160 How anemic were you, Sarah? I was like six at this point. I mean, it was bad. Really bad. The low

02:01:15.160 sixes at this point. Right. And just so the listener understands, the normal would be 13 or 14 of a

02:01:21.200 hemoglobin and you're six. So that's really low. And your platelets were how low?

02:01:25.740 23. Which means you basically don't have the ability to form a single clot.

02:01:29.980 Right. I was a disaster. And the funny thing is I was still up and doing okay. You know what I mean?

02:01:37.780 I was tired. I was shortness of breath with activity, but I was doing okay. And they sent me home.

02:01:43.080 And I was like, that doesn't seem right. Am I crazy that I shouldn't be home? So of course I call some

02:01:53.580 of my other physician friends. Aha. Privilege. Right. Because I was getting sent home. And they're

02:02:00.900 like, oh my God, we're admitting you right now. So I actually get a backdoor admission to the hospital

02:02:07.400 hospital. And a complete workup starting right then. I had to have a thoracentesis. Drained a

02:02:13.740 whole bunch from my lungs. That was unknown when I got sent home. So you had tons of fluid around

02:02:19.520 your lungs. Tons of fluid around my lungs. That's obviously explaining the shortness of breath.

02:02:24.060 Yeah. And once I was admitted, I was promptly transferred to ICU. Things were going downhill.

02:02:30.420 I had to be put on BiPAP. So I had multi-organ failure. Had respiratory failure, liver failure,

02:02:36.460 kidney failure. I was a big failure. Okay. Everything was bad. And was this believed to

02:02:42.460 be the result of your body's response to the tumor or the chemo? It was the GEMSAR. So I got taken care

02:02:51.640 of in the hospital. I just want to cry to think about the care I got. It was so wonderful. And I just

02:02:59.580 had the best team. I would have died. Nobody can believe that this was well over a year ago now.

02:03:08.580 And I'm healthy with no persistent failures because I was near death. And I was in the ICU for a really

02:03:18.960 long time. And everyone, every day, it went from, I think your kidneys will rebound to

02:03:24.720 50-50. They're never going to be normal. I was on plasma phoresis and it turned out I had something

02:03:35.480 called atypical hemolytic uremic syndrome. And to just explain, over 70% of people are either dead

02:03:42.940 or on dialysis right away. I mean, it's got an incredible mortality rate. Incredible. It's

02:03:51.940 incredibly difficult to treat. And so outcomes are you're dead or you're on permanent dialysis.

02:04:01.000 So I was put on a new medication after going through kidney biopsies, all these kinds of things

02:04:08.080 in the hospital, sent home, did outpatient plasmapheresis for a while. And then things

02:04:15.760 miraculously started getting better, right? Not miraculously. It was because of this medication

02:04:19.700 I was put on. Of course, that meant an infusion every eight weeks. And the worst part to me is it

02:04:25.260 meant no one would put me back on chemo. Just they wouldn't put you on GEMSAR or they wouldn't put you

02:04:29.820 on anything? Wouldn't put me on anything. And to me, that was devastating because I said,

02:04:35.140 well, kidney failure is one thing, but having this cancer that we know come back is another.

02:04:42.200 So that was another hard pill to swallow. And long story short, I got better. I went to

02:04:50.300 pharmacogenetics, which is where they actually take a look at what your genetic profile is in response

02:04:56.940 to different drugs. And it turns out I had a genetic mutation. Hey, I have lots of them.

02:05:03.980 It turns out I had a genetic mutation that didn't allow the GEMSAR to break down. So I was getting

02:05:11.340 toxic doses of this. And I was on a very low dose. But the thing is that I couldn't get rid of it.

02:05:19.060 So normally, if you see atypical hemolytic uremic syndrome with GEMSAR, it's after months and

02:05:24.440 months of treatment. And I got this within four weeks. Why? Because I was getting mega doses of it

02:05:33.240 because my body couldn't get rid of it due to this mutation was the explanation. You know,

02:05:38.840 and they said, there's no reason you can't take any other chemo. This is very specific to GEMSAR.

02:05:43.860 But that was that. Sit and wait mode. Back to sit and wait mode. And it took another year,

02:05:55.000 but the cancer came back in September of 2020.

02:05:59.600 And here's my story from that, which really made me so determined to work even harder for health

02:06:12.660 equity. Here I am, a physician, able to grasp really difficult concepts, able to read and scour

02:06:22.540 the literature and know what I'm looking for, able to call at a moment in time, you know, any time,

02:06:28.340 someone to help me sort through something I didn't understand or help maybe refer me to

02:06:35.440 someone. You know, I had all the resources in the world. And the reoccurrence was in September.

02:06:45.840 Even with all my constant pushing and self-advocacy, the one thing is I had, by the time I was diagnosed

02:06:54.720 with cancer, I was an expert patient advocate. Expert. Hardcore. And, you know, one of the other

02:07:03.700 advantages I had is it didn't take much to switch that and to become a self-advocate, an advocate for

02:07:08.880 myself. So I was diagnosed in mid-September with a reoccurrence. I did not get on a clinical trial

02:07:18.660 until I got started December 30th. That's a four-month delay. That's a four-month delay

02:07:28.840 for me. And in hindsight, now, looking back, before I was panicked, right? And I couldn't really,

02:07:38.800 I was like, something has to get done. Something has to get done. Something has to get done.

02:07:42.440 I can look back in hindsight and say, how many people die during that time?

02:07:53.520 How many people who don't have the advantages I had just die during that delay?

02:08:01.500 How many? I shudder and I just want to cry. And what I've done is I've reached out to other cancer

02:08:10.120 patients to say, has anyone else been in this situation? And I find out it happens all of the

02:08:18.900 time. It seems that we have a really good system. As I experienced, when someone is diagnosed with

02:08:26.040 cancer, they get a health, a cancer navigator, you know, they get all these things and we're boom,

02:08:32.600 boom, boom, boom, boom. But when that cancer comes back, it's kind of like the system seems to give up on

02:08:36.920 you. I had to advocate, advocate the heck out of getting a biopsy done. A biopsy that would be

02:08:46.500 enough tissue to make me eligible for a clinical trial. That would actually get me a full genomics

02:08:53.800 report. I mean, that wasn't going to happen. I'm telling you, I had to get almost obnoxious about it.

02:09:01.220 And the stories that I'm getting from people are the same.

02:09:06.700 Where was the recurrence?

02:09:08.300 In my right upper lobe.

02:09:10.220 So they had to get, you had to get another lung biopsy to do this. And can I ask you another thing,

02:09:16.580 Sarah, what has been, you obviously have health insurance, but I assume that there's been

02:09:21.340 a non-trivial amount of out-of-pocket costs as well in the last four years?

02:09:25.900 Oh yeah. Oh yeah.

02:09:28.200 Do you have a sense of what the out-of-pocket cost has been for your care?

02:09:33.040 Tens of thousands of dollars.

02:09:34.860 Which obviously speaks to another challenge. I don't know if this is still true, but

02:09:39.460 it certainly was true at one point that the greatest source of personal bankruptcy in the

02:09:45.740 United States is healthcare and inability to pay healthcare costs.

02:09:50.080 And a cancer diagnosis is so high up there.

02:09:54.040 I would have to believe that cancer is the leading subset of that as well.

02:10:00.060 So now I'm like, especially when I got feedback that I'm not alone in this. It wasn't just me,

02:10:10.440 you know? And again, I always keep saying in the backdrop of, I am one of the privileged.

02:10:16.480 And I was put in this situation. And the fact of the matter is by the time the reoccurrence was

02:10:22.140 diagnosed to the time I finally got treated, I had progressed so much that I had compression of

02:10:31.700 my bronchus. I couldn't get up a flight of stairs without desaturating. I mean, this all just happened.

02:10:36.720 I was in horrible shape, which of course, again, and remember, I'm starting out before my diagnosis

02:10:45.640 in general, I was so healthy, which gives me an advantage in this, which gives me a significant

02:10:53.340 advantage in this. But it goes back to that question of how many people just die.

02:10:58.160 Sarah, you're very realistic about the fact that your time on this earth is less than it should

02:11:07.780 be, right? A 49-year-old, otherwise healthy person who's done all the, you know, done the right

02:11:16.080 things for their health should have another 40 years on this planet. And at least statistically

02:11:21.160 speaking, that's, that's not, doesn't seem likely. It suggests to me that you're very cognizant of how

02:11:28.200 you spend your time. So should take a moment to thank you for spending a couple hours with me here.

02:11:36.400 But how do you now think about the time that you allocate to your family, to your work in the

02:11:45.640 diabetes community, and now to this third important pillar to you, which is cancer advocacy?

02:11:54.160 How are you managing that? And how do you, how do you think about how to even balance that? Because

02:11:59.400 I think time is the most important currency. I think everybody can appreciate that in a vague

02:12:05.660 sense. It is the great equalizer. But of course, most of us can't appreciate it the way you can,

02:12:13.080 because you have a real visceral appreciation for it that comes exactly with this type of an illness.

02:12:21.300 And so therefore, I think that your appreciation for the balancing act of what you described earlier,

02:12:28.760 which is living your life to the fullest, regardless of its duration, that's your legacy. That's what

02:12:35.780 your kids are going to remember about their mom being the advocate for other patients so that in 10

02:12:42.220 years, when another Sarah Halberg gets this diagnosis, even if she doesn't have your education

02:12:48.540 or your means, she can have an extension of life the way you do. It's a bit overwhelming for me to

02:12:55.160 think about how I would do that. Because as I put myself in your shoes, my intuition is I'd want to

02:13:00.280 retreat from everything outside of life, everything outside of my family. Like I would imagine, and it's

02:13:06.360 hard to put yourself in another person's shoes without being there. But my intuition is I would say,

02:13:11.020 I don't care about anything outside of the walls of this house. And I would take a selfish approach

02:13:17.140 in some ways, I think. And you've done this very selfless thing, which is continuing to sort of

02:13:23.060 prioritize everything else as well. How do you do that? A couple of things. Number one, believe it or

02:13:29.480 not, originally, it was actually hard to be around my kids. When I was so deep in grief, because

02:13:36.880 and that sounds crazy, right? That sounds counterintuitive, but they reminded me of

02:13:42.700 everything I was going to lose, right? They were what I didn't want to lose. And so it was challenging.

02:13:49.920 And I knew I had to overcome that. That was a big motivator for me to not be thinking about that

02:13:56.200 and thinking in that way. And I'm happy to say I clearly have overcome that. But my kids come first.

02:14:04.180 I'll drop anything and everything if they need me now. But I also think, again, and I go back to

02:14:10.960 sort of what I alluded to before, they need to see me not getting knocked out by the stressors and bad

02:14:21.960 things in life. I mean, bad things happen to good people. Like I said, there's been a pivot in every

02:14:28.260 part of my career based on anger. And I certainly am angry about this. But what do you do with it?

02:14:34.180 That's what's going to be the important question in life. You can take anger, you can take all these

02:14:39.880 things, and you can get lost and buried in it. Or you can try to turn it into something else.

02:14:47.540 And I have to say, I haven't become as big a cancer advocate yet. And I'm working on it.

02:14:54.700 But the reason for that is, and this was a question I had to ask myself a long time ago,

02:15:00.020 which is, shouldn't you be a cancer advocate now? But I have a platform for diabetes. And damn it,

02:15:07.040 that's important too. All these people suffering from this is important. So I can't just say, 0.98

02:15:13.120 I'm going to switch away from a platform that I have to one where I don't yet. It doesn't mean

02:15:18.640 I'm ignoring it. But it's like, it makes me want to work more again for health equity,

02:15:26.020 because it spans both, right? It has to do with both diabetes and cancer. And that is so important.

02:15:36.760 So yeah, how I spend my time is really critical. And I want to say, it's not like I'm,

02:15:43.520 I don't want to paint the picture that, oh my gosh, I'm the superwoman. I have a terminal cancer.

02:15:49.580 And yay, life is great. No. When people ask how I'm doing, okay. If I say, okay, you know,

02:16:00.080 I'm doing okay. There's never good or never great. Okay. And that's just where I live right now.

02:16:07.160 I'm definitely not sitting around and feeling sorry for myself. Okay. Definitely not,

02:16:13.140 not enjoying things in life. But great is hard to think about. You know, great is hard to think

02:16:21.240 about now. And some people say, well, so cancer really helped me get a new perspective on life

02:16:27.240 and what I care about. And I'm happy to say, I don't know that I got that. Okay. I mean,

02:16:33.800 having cancer sucks and I'm still mad about it. And you know, sometimes I have to sit and have a 0.95

02:16:41.520 pity party every once in a while because the fact of the matter is I loved my life pre-cancer. And I

02:16:48.240 think I was living every minute of it. I think I cherished my children. I cherished vacations. I

02:16:54.560 mean, you know that I cherish travel and showing my children travel. That's a bit of a wonderful thing.

02:17:00.360 And it's also like a dagger too. It's not like I've gotten some new life and new perspective

02:17:06.360 that's so different from my old, dammit, I liked my old life. And I liked the old me. And it's still 0.86

02:17:12.980 a little hard to get used to who this person is now. She's still motivated. She still exercises.

02:17:20.080 Although not doing the things I used to. She loves her children with as much passion

02:17:28.080 as one could have. But I'm fundamentally different. It's tough.

02:17:34.080 Sarah, you've said a lot of things that obviously resonate. And I think will resonate with a lot

02:17:46.920 of people. So I want to thank you from the bottom of my heart and certainly wish you the best.

02:17:58.080 Thanks. I appreciate it.

02:18:01.200 It's been great knowing you through this journey as well. You are, uh, as many of your colleagues

02:18:07.120 have undoubtedly told you, and we've certainly discussed it behind your back. You are an

02:18:11.920 inspiration and nobody wants to hear that because nobody wants to be the inspiration. You just want

02:18:15.920 to be the normal person, but you are an inspiration. I just want to be a normal person. Yeah.

02:18:21.280 Well, thank you for setting aside time.

02:18:23.300 Yeah. And I mean, I thank you so much for having me on. I mean, believe it or not,

02:18:28.340 this is the first time I've told my story in any way, shape or form. So I have been kind of

02:18:36.340 preparing for this and I'm glad I did it. So thank you for giving me an opportunity to do that. And

02:18:45.780 thank you. Thank you for trusting us. Thank you for trusting me and the listeners.

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02:21:21.940 Declate Tate.

The Peter Attia Drive - May 17, 2021

#162 - Sarah Hallberg, D.O., M.S.： Challenging the status quo of treating metabolic disease, and a personal journey through a grim cancer diagnosis

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