The Melanie Avalon Biohacking Podcast Episode #246 - Gary Taubes

TRANSCRIPT

(Note: This is generated by AI with 98% accuracy. However, any errors may cause unintended changes in meaning.)

Melanie Avalon:
Hi friends, welcome back to the show. I am so incredibly excited about the conversation I am about to have. So the backstory on today's conversation, I've had this guest on the show once before, which was such a surreal honor, and I can't even believe it's happening again now. It's sort of funny. I was telling this guest this story beforehand, but I recently interviewed a mutual friend, Dave Asprey, and he told me, I don't know how it came up, but it was very random. And in the interview, he said that one of the reasons he's really doing what he's doing today is that the fantastic Gary Taubes introduced him to his book agent. So not the same glamorous story like that, but I am also doing partly what I'm doing today because of Gary Taubes. I read way back in college, I have it right here. And since this is video, I get to show good calories, bad calories. Can people see that? And it actually still, I was looking through it. This was old school back before we were doing audiobooks and Kindle. It has all my highlights still and all my notes. This book changed my life. I had found the low carb diet and read that book and the science and the history and just the depth of everything I learned was such a paradigm shift, so mind blowing. Honestly, like I said, it's probably the reason that I became obsessed with the science of diet, if that's a topic. And so since then, I've been following all of his work. He is an acclaimed journalist. I'll put his bio on the show notes. He almost needs no introduction, but he's everywhere and he's written so many books since then. So he wrote, like I said, good calories, bad calories. He wrote Why We Get Fat and What to Do About It, which was sort of like the... Would you say that was like the good calories, bad calories for the more general population?

Gary Taubes:
I describe it as the airplane -reading version of the book, okay? So it can be written, read between Atlanta, for instance, and say Salt Lake City, if you were flying out to California, and you're a fast reader.

Melanie Avalon:
That makes sense. I was actually thinking, because your newest book, Rethinking Diabetes, What Science Reveals About Diet, Insulin, and Successful Treatments, it came out in January of 2024, I was actually reading the Amazon reviews. I don't know if you read Amazon reviews for your books.

Gary Taubes:
I used to.

Melanie Avalon:
stop that habit. Yeah. Okay. So in any case, I was reading some of them and what I was thinking was a lot of people were talking about how it was, you know, amazing and very long and intense. And I was like, I wonder if he'll make like how he made why we get fat version of good calories, bad calories, if he'll make like the version of rethinking diabetes for this.

Gary Taubes:
But oddly enough, and by the way, Melanie, thank you for having me on the show. The previous book, The Case for Keto, was already kind of the why we get fat for the diabetes book, although in Case for Keto, I'm talking about obesity and diabetes. But yeah, the rethinking diabetes is a return to a very kind of dense, lots of history, lots of philosophy of science, how to do science right. I recognize as I wrote it that I was writing it more for myself than your typical patient with diabetes or just with an interest in nutrition and health.

Melanie Avalon:
It's incredible. It is a lot. I learned so much. It really is rethinking. I mean, you really rethink diabetes when you read it. And actually, to that point, because I was going to ask you, you know, what made you decide to write it, and you kind of sort of address that, I'm super curious. When you sat down to write it, and then you did all the research, you wrote it at the end, your own paradigm shift, or biases, or interpretations of everything, did you have any really significant shifts, or did everything sort of, did you find what you were looking for?

Gary Taubes:
I mean, the steak is full of things that were revelatory to me. So one way I think about this, I now think about it. So imagine like the nutrition disease picture that we're interested in is a thousand piece jigsaw puzzle and physicians at any point in time, the further you go back in time, the more influence they had on everything that comes afterwards and the fewer pieces they had to draw their conclusions. So like in the 1920s, after the hormone insulin is discovered and we'll discuss, it's like we have this thousand piece jigsaw puzzle, they have 50 pieces of the puzzle and they're drawing conclusions about how to treat diabetes, what this disease is, what the mechanisms are involved and that in fact, everything we believe ever after from 50 pieces. Now, largely because of the internet and medical publishers and these databases, you can get virtually every article, every textbook from 100 years ago. So you can see, I don't know, I'm guessing 900 of the thousand pieces. So you get a much more comprehensive view of what was known and what wasn't known and you can see what they should have concluded back when they only had 50 pieces. So there are entire aspects of the story that I had no idea about when I started. And some things that I had these sort of vague ideas about, like I read a little about the role of glucagon and this guy, Unger's ideas that glucagon dysregulation is more important than diabetes than insulin. And I had developed in doing good calories, bad calories, a sort of obsessive appreciation for the role of the liver in all these metabolic diseases. But I had no idea that in diabetes research, you know, it starts off in 1921 when insulin's discovered, everybody thinks this is a insulin deficiency disease and the organ responsible is the pancreas. And that's kind of true for type 1 diabetes, which is maybe 5% of all cases. But for the other 95%, the liver plays the major role in that this was worked out by the 1940s and had zero influence on how diabetes, diabetologists will call them the researchers who study it and the physicians who treat it thought about the disease and treated it even though the physiologists had concluded that the liver was a problem, so they had the wrong organ. And they had the wrong disease for 95% of all cases and it had zero, effectively zero effect on how they treated it. I never imagined, yeah, you're treating, right, when you're giving insulin or pills, oral hypoglycemic agents, you're targeting blood sugar, right? You're trying to lower and control blood sugar. That's why we wear continuous glucose monitors because we want them to see. So I had no idea. Never crossed my mind until the 1960s. No one had ever really measured how blood sugar responds to our foods and our diets because they couldn't measure blood sugar. They had to take a blood sample and send it off to a laboratory. So you'd get, like, a patient would come in, you'd take a blood sample, you'd send it off to a lab, and two weeks later you'd tell him what his blood sugar was when he came in to see you. And when he came in to see you, he had changed his diet for two or three days before because he knew it was blood test. So they had zero information, feedback on how their therapies were working. And nobody really thought about that at the time. They couldn't measure, they were treating a disease of insulin resistance. There's too much insulin. They couldn't measure insulin until the 1960s. So it's like, anyway, those are the kind of things when you start realizing that, you realize how little people really knew. And the belief system and the philosophy and the way of thinking about the disease that these people created with such little knowledge and so incorrectly still largely determines how we think about it today. So long answer to your short question, was there revelations? Yes.

Melanie Avalon:
You touched on so many things I'm going to talk about and okay, so many questions from what you just said. And I think listeners can understand now why they really need to read this book and have their minds blown about everything. So actually, because you were talking about this a bit throughout that, which is, you know, they were treating the wrong disease in a way or, you know, seeing it as different things. And so even the word diabetes, like we have type 1 diabetes, type 2 diabetes, I've even heard there's like type 1 .5 and type 3. That word, is it kind of similar to, you know, like the word fat and we have body fat and dietary fat, but people see them as the same thing, but they have completely different roles or like with iron, like we call iron deficiency anemia and we call iron overload, you know, hemochromatosis, I think, diabetes, is it even the same thing? Like type 1 diabetes and type 2 diabetes, or is it a completely different disease?

Gary Taubes:
Arguably, they are completely different diseases, and now let me give you, as I tend to do when I come in this book, the long historical story, again, from this was a diabetes of any kind was an extremely rare disease through till late 19th, early 20th century. If you're a physician, a typical physician might see one or two cases in their lifetime among their patients. And the 19th century, they recognized already that there were sort of two forms of the disease because there were two types of patients. There was young patients who, you know, for whom the disease was sort of an acute disorder and it killed them quickly. And then there were older patients and heavier patients for whom the disease seemed to be more of a chronic disorder and it killed them slowly. But in both cases, the patients would kind of present it aside from the different grouping of the patients, they would present with similar symptoms. Because in type two diabetes, like today, we'll diagnose it from a blood test. So you go to the doctor, you get a blood test, they say your hemoglobin A1C is over seven, diabetes, or it's over, you know, six, pre -diabetes, or you're moving toward diabetes, but back then they didn't have blood tests, they didn't have these chemical analyses. So nobody knew they had diabetes until they started manifesting the symptoms and the symptoms were kind of the same. So you're hungry all the time, called hyperphasia, you're thirsty all the time, you're drinking enormous amounts of fluid, you're peeing all the time, you're losing weight, I mean, you know, emaciated. So the patients with both types of diabetes would see the doctors at a stage when their symptoms were very similar. And then they would get them one of the ways that doctors would diagnose it other than the symptom presentation as they would, you know, again, they didn't have the sophisticated chemical tests. So they would have their assistant taste the urine, that was a diagnostic test pre 20th century. And if it tasted sweet, that would confirm the diagnosis of diabetes. And then the treatment was aimed at what they call de -sugarizing the urine. So if you could get all sugar out of the urine, and even in the 19th century, they did have chemical tests also to see how much sugar was in the urine. If you can get the urine sugar free, that was considered successful treat, had no idea what was happening with blood sugar, they didn't know that the urine sugar is the sugar content, the urine reflects blood sugar content hours and hours before, they just knew that that was a symptom, if they can make that symptom go away, they had the disease. So 1921, 1989, is more one of the most famous experiments in diabetes history. German name Minkowski demonstrates that if he removes the pancreas from a dog and keep the dog alive, which nobody thought he could do, they can do the dog will develop diabetes. So from 1989, it appeared to be a disease related pancreas. And then in 1921, this team at the University of Toronto led by Banding and Best discover insulin, and they show that it's a very powerful and they they purify it from calf pancreases. So that confirms the idea of Minkowski that this is a pancreatic deficiency disease. And then they show that insulin therapy does like miraculous things with patients, even in the latest, you know, the stages of diabetes where they're basically hours or days away from death. And all of this locks in the idea that this is a pancreatic deficiency, insulin deficiency disease, but They never seems to cross their mind that that's only true for the acute cases for what we call type 1 today. And then, as I said, as time goes on, they recognize, you know, by the 1940s that the liver is playing the major role in type 2 diabetes. You can't really, if you remove the liver from animals and keep them alive, you can't really give them diabetes, and we could discuss why, what the role of the liver is playing. And the hormone glucagon is playing a critical role by stimulating insulin secretion of glucose by the liver. Then, like I said, by 1961, they finally have a technology available to measure hormones in the bloodstream accurately, and now they can finally measure insulin. They see that type 2 diabetes is a disease of too much insulin, not too little. If you put it all together, yeah, it's an entirely, it's the liver and not the pancreas. It's too much insulin rather than too little insulin. It's basically glucagon driving this disorder or driving one of the symptoms, high blood sugar or not, insulin, but it doesn't affect how they treat it.

Melanie Avalon:
This is so crazy. I remember the first time, I don't know where I heard it, but I read that when people have high blood sugar that it's primarily actually from the liver, not from what you just ate. That was such a shock to me. And I was like, how does nobody, even today, nobody really talks about that. I mean, we talk about the role of the liver producing sugar and all of that, but we're always focused on what we're eating more so, I think. And so learning in your book, and you just mentioned both of it now and in the beginning, this idea that you can't even have high blood sugar, so have type two diabetes without the role of the liver or glucagon is just mind blowing to me. And so can you talk a little bit more about glucagon? And because just now you were saying that the role of glucagon, but you talk about in the book how insulin, or it does affect glucagon, right? It's affecting,

Gary Taubes:
Oh, yeah, absolutely. So this was sort of mind blowing, and I couldn't actually believe I was writing these chapters, because when you go back in the history, like someone you have 900 pieces of puzzle instead of thing, you can see where mistakes are made, you can see what people weren't seeing, and how they were reacting to what they could see incorrectly. So the first mistake, the whole science of endocrinology of hormones kind of dates to 1869 when a famous French physician says he's purified, but would have been testosterone. Bowles test dog testicles, and he's injected into himself, and he's rejuvenated himself with primitive testosterone therapy. And this is kind of the beginning of the science of endocrinology of hormones and hormone related disorders. And then it's there are various discoveries, like, you know, that thyroid produces thyroid hormones that seem to have an effect on metabolism. And this pancreas produces insulin that seems to have an effect on glucose, blood sugar levels, and sugar in the urine. And so by the 20th century, the science of endocrinology and hormones is evolving and developing. And there's maybe a dozen physicians in the world, most of them in Germany and Austria, who really understand what this is starting to tell them. But the whole science is based on this idea that there's an organ that secretes a substance that then works elsewhere. So an endocrine disease was considered a disease that was one of the organs is defective. So like the pancreas and diabetes is an endocrine disease because a pancreas is not secreting insulin, or my exedeme is thyroid disease because a thyroid isn't secreting a proper hormone. And so whenever they wrote about this in the endocrinology textbooks would include chapters about how hormones were sort of the crucial element in maintaining what we call homeostasis. So maintaining the proper conditions in the internal environment of the body such that our body functions properly. But when they wrote about it, they would write about it for the perspective of, you know, what does the pancreas do? What does the thyroid do? What are the testicles do? What is, you know, the female sex hormones do? And what diseases might be created when these organs are defective? When they had no idea that the dysregulation could happen, not just where the hormone is secreted, but it could happen at the receptors of the cells or the tissues where the hormone is received. That's what insulin resistance is, right? It's not a problem with the secretion of insulin. It's the problem of other cells in the body sensitivity to insulin. So the entire science of endocrinology, on one hand you've got these very smart physiologists who are really thinking deeply about this and writing about the complexity of homeostatic systems and the role of hormones and the central nervous system primarily and controlling these systems. And then you've got the medical textbooks that it's just, it's all about the hormone and the organ that secretes it and the disease that might be caused by it and nothing else. So one of the ideas here is in endocrinology, the physiologists are writing about is how every hormone is going to have counter regulatory hormones, counter regulatory effects. So a hormone that does something on one cell is likely to do something else on another cell to, as a negative feedback loop, to keep it from running out of control, to keep the, you know, equipoise in the system. And just as 1921, they discover insulin. Well, by that time they've discovered what are called the beta cells in the islets of Langerhans. So they establish that insulin is secreted by these beta cells and that it lowers blood sugar. That's one of the more obvious things it does. They also, researchers like a year later, discover the hormone glucagon and establish that it's secreted by the alpha cells of the pancreas. That happened to be right next door to the beta cells and pretty much everything insulin does glucagon does the opposite. And so when insulin is secreted, it stimulates HUCCA and as time goes on and they talk about how these hormones work, and this was fascinating to me because it's kind of the whole beginning of the world of systems biology. So when your blood sugar is going up and it stimulates insulin secretion and insulin's secreted by the beta cells, so the cells that see the very highest dose of insulin are the alpha cells next door that are secreting glucagon. So they're the first thing to respond, and in the insulin and the glucagon, so the insulin stimulates glucagon secretion to immediately begin to balance out the effect it's going to have. And as the insulin and glucagon go through the portal vein to the liver, the liver sees the next highest dose of both drugs, and the glucagon, by the way, inhibits insulin secretion. So again, you've got all these negative feedback loops being created almost instantaneously in effect to maintain the system and homeostasis and balance. Half of the insulin never gets out of the liver, so half of its action is happening in the liver, and the question is, what's it doing? And the glucagon, its second aid that did organ that sees the second highest dose is the liver, and what the glucagon is doing, insulin is telling the liver cells to take up blood sugar, and glucagon is telling them to secrete blood sugar into the bloodstream. And the blood sugar levels elsewhere in the body are basically determined by this balance, and this is all stuff that's worked out over by the 1970s mostly, and I could then just follow Unger if Unger at the University of Texas played a major role. The blood sugar elsewhere in the body is the balance of insulin of the blood sugar taken up by the cells minus the blood sugar that's secreted back into the cells by glucagon. And insulin is supposed to, excuse me, earlier said it stimulates glucagon secretion, I should have said it inhibits glucagon secretion. By inhibiting glucagon secretion, it's supposed to inhibit the secretion of blood sugar from liver cells into the bloodstream. So the idea is you've eaten carbohydrates, your blood sugar goes up, you want to shut off this system for supplying blood sugar to the blood when you haven't eaten any carbohydrates or haven't eaten, but if you're insulin deficient or insulin resistant, that inhibiting the effect of glucagon fails. So yes, you've got blood sugar going up because you've eaten carbohydrates in your diet and you don't have insulin stimulating your cells to take it up and use it for fuel, but the main reason insulin is going, blood sugar is going up is because the insulin is supposed to inhibit the action of the glucagon and the glucagon stimulating, just keep getting this wrong. I mean, I need my own AI to keep these things in line for me. Insulin is not inhibiting the action of glucagon, so the glucagon is continuing to tell the liver to secrete glucose into the bloodstream when you don't need it. So the reason your blood sugar is high is, you know, you could argue in part immediately after the meal because of the effect of eating a carbohydrate rich meal and not having insulin stimulate, facilitate, uptake, but the major reason is because it's not doing the job of inhibiting glucagon, so glucagon is still telling the liver to secrete glucose into the bloodstream even when you don't need it. It's like if you, let me see if I can get a bathtub analysis going. You don't want your bathtub to overflow and you've got a drain that's taking the water out and insulin is telling more and more water to go out and glucagon is telling more and more water to go in and from the faucet and the insulin is supposed to stop the glucagon and so in effect turn off the faucet that fails to do that. So the major reason why your bathtub overflows is because the faucet is still pouring water into it and the major reason why you have high blood sugar and diabetes is because your liver is still secreting, it's doing de novo on glucogenesis, it's creating sugar and dumping the blood treatment is not to post it. And yeah, nobody, I too read about this. I bet you Mike Eads probably wrote about it 20 years ago because Mike sees all this stuff before we do. And the role of glucagon, I had read about occasionally. I think Richard Feynman had also written about it, but I didn't take it seriously because the claims were so dramatic. You know, the reason for the high blood sugar and diabetes is not the carbohydrate rich diet, but the failure of the liver to shut off de novo glucogenesis. And then when I started reading all the literature, they used, I mean, you see it, you see the hypothesis be raised in the literature. Then you see the conflict, you know, lasting 10 or 20 or 30 years. And then you see who wins. And in this case, pretty much everyone agreed that the problem was glucagon and the failure to inhibit stop the liver from secreting glucose into the bloodstream. And didn't, nobody cared, had no effect. And if you were to go to the NIH website today, it would basically describe the science as it was known in 1925 is that none of this happened.

Melanie Avalon:
It's funny, I, I as well kept getting, I keep getting like confused with it. I think it's so confusing when you're talking about something that is stimulating the inhibition of something, which is stimulating something. It's like a lot of circles to like keep straight. Okay. So basically, so let me see if I can say it and let me know if I have this correct. So insulin, I really like that bathtub analogy. So insulin, or no, I'll start with glucagon. So glucagon stimulates the release of sugar from the liver. So that can create high blood sugar. When insulin's released it first, before actually anything else, it comes out of the, the beta cells and then the neighboring alpha cells that are, you know, controlling glucagon see that or are affected by that and so then glucagon stops. So now we no longer have that stimulating effect of blood sugar coming from the liver, so we shutting that off. And then also insulin is sort of affecting the drain. So it's also like putting away the sugar. So it's kind of affecting two different things there.

Gary Taubes:
Yes, another misconception is that you need insulin to use blood sugar and for yourselves to metabolize blood sugar and you don't. Insulin, the way, you know, it facilitates the uptake and makes it easier. It increases the amount of glucose that they'll burn, but they can use, they can do it without insulin. So it's sort of, you know, and again, if you think about it, so you eat carbohydrates and the body kicks in this system to keep blood sugar on the control. I mean, arguably the major problem because high blood sugar levels are toxic. That's one explanation for the, all the complications that associate with diabetes and that work particularly fierce and acute when during the years you know, prior to insulin therapy or the first 20 or 30 years when insulin therapy was, was so poorly understood. So your body's trying to prevent blood sugar from getting too high and or too low. One of the points Unger makes when he writes about glucagon is, is that high blood sugar is, causes chronic disease and death, but it does it slowly. Low blood sugar could be immediately fake. So you have also a very powerful system to prevent low blood sugar. And that's what glucagon is doing. So insulin is kind of preventing high blood sugar and glucagon is preventing low blood sugar by telling the liver and effect keep pumping out glucose. But then the other thing is, yeah, we're just talking about the liver. So, well, there are a few things that I were fascinated, you know, a point Unger made other researchers, clinical investigators had made it earlier. Is that, you know, when I said the insulin secreted by the pancreas, you see a very specific dose response where the alpha cells see the highest dose and liver sees the next highest dose. And then it gets out the general circulation and only half of what's secreted get out general circulation. When you inject insulin and it's therapy and it starts in the general circulation, you get an entirely different dose curve. So then you have to give a ton of insulin, particularly if the patient is insulin resistant to eventually have the same effect in the liver and in the pain, and the, and the beta send the alpha cells. So now, even if insulin is benign, or I mean, we can't live without insulin when it's, you know, from the pancreas, but when you're, when you're injecting it into your body, your abdomen or your thighs, and it's, it's percolating through the circulatory system you're having in your, these, all the organs are seeing entirely different. They're seeing non -physiological doses. And because you have to give such high doses to have the proper effect in the liver and at the pancreas, you end up having way too high of doses on physiological doses in the circulatory system, where you're manifesting a lot of the chronic locations of the disease. So one of the conclusions I came to, which in some circles in the diabetes physiology communities as well, except that this is the argument on germane, which is basically you could never safely give insulin therapy without doing chronic damage and also without causing low blood sugar and having hypoglycemic episodes and the more insulin you gave, the more likely you'd have hypoglycemic episodes because the insulin stays in the circulation longer. So it inhibits the glucagon longer and you don't get the glucagon protecting you from low blood sugar. So there's all this world of issues come into play when you start accounting for all the wonderful, a complexity and manifestation, like the real, the reality of these diseases instead of this sort of cartoon, 50 pieces of the thousand piece puzzle version that physicians originally learned in the 1920s and then never really got themselves away from.

Melanie Avalon:
Are you saying that when we put the insulin directly into the bloodstream, it will initially, or it will eventually make its way and affect the alpha cells, but it just requires a lot more because it's not there. It's not originally coming from that location, like right next door.

Gary Taubes:
Yeah, you have to put in a lot more. You have to use a lot more to have that effect. And when you use a lot more, that's also stays in the circulation longer. And then again, depending on what kind of insulin you're using, if you're using long lasting insulin, the insulin, the half life, the insulin, and then the circulatory system worked much longer. So when it finally has one on glucagon, it could be 12 hours after you took your injection, when they first invented, when a long acting insulin was first invented, this was like 36, 37. For many people was seen as a, as, you know, a paradigm shift in diabetes therapy, because now you had an insulin could just take one twice a day, ideally once a day in the morning and patients would take it in the morning and they have, you know, a hypoglycemic episode while they were asleep at night, because now they were hours and hours away from having eaten their last meal and any carbohydrates or glucose from that meal, and the insulin would still be circulating bloodstream. How inhibiting glucagon, glucagon should be, you know, causing some secretion of glucose and from the liver to, you know, maintain a healthy blood sugar level. But it's true. I, there are these, you know, negative feedback groups on top of negative feedback loops on top of, you know, like hormones and counter regulatory hormones and counter counter regulatory hormones. And that's what homeostasis is. I mean, it's just incredibly complex system. I think of it as a sort of spider web with thousands of webs and it keeps the, this is what Fod Bernard sort of invented the concept set 1865. Basically it's, it's the whole, all of human, all of life is about maintaining the, the constancy of the internal milieu of the cells. So you're not just keeping the body alive. When you're keeping up an organism alive, you have to keep the individual cells alive, the cells only see what's immediately outside of their cell membranes and the cells, you know, around them. And then if there might be a nervous system connections to the cells, but they're getting everything they need to live from the, the milieu, but directly outside the cells. And so that all of this system, when we talk about a homeostatic system as Bernard said in 1865, it's designed to keep that milieu relatively constant. It's like our cells are, yeah, they're naked people walking around outside. That's they're going to stay alive. They better and healthy. They better live like in Oakland, where I am where 65 degrees and sunny all year round because of it diverges from being 65 and sunny. They might drive die from, from, you know, cold exposure or heat exposure, you know, whatever. So that's the whole system is the buying to keep that internal milieu constant, relatively constant. You perturb it the way you prevent it from being seriously perturbed is all these negative feedback. So hormone that does one thing also kicks into action, a hormone that does the opposite and the hormone that does the opposite in turn kicks, you know, triggers at that first hormone.

Melanie Avalon:
to that point, what are your thoughts on the role of time with the homeostasis? And what I mean by that is, because you were just talking about how with hypoglycemia, there's all these different potential hormones involved to prevent us from getting that. But with hyperglycemia, it's really just insulin. And the effects from that are, it's like negative health effects down the line in the future. So it seems like the body is really intensely acutely aware of the present moment in maintaining homeostasis, but does it have a perspective of the long term? Because you would think in a way it doesn't, because it doesn't seem to, quote, care as much about hyperglycemia. But at the same time, we seem to store a lot of fat to prevent from future starvation, which that would be a long term homeostatic thing. Yeah, what are your thoughts on the perspective?

Gary Taubes:
Okay. So we're going to have to get back to the fat and protecting from starvation. But yeah, the body knows. And again, this is as a system, as the science progressed, 1920s onwards. I described sort of how the primitive state of the science in 1921, when insulin discovered and then glucagon is discovered, I think the year after, and the growth hormone is discovered around 1922. So they have all these ideas basically about diseases of too much or too little hormone because they can sort of see the effect. You know, too much testosterone or too little, too much growth hormone or too little with growth hormone. You know, if you have a tumor in the hypothalamus, not the hypothalamus, a pituitary gland of a giant, then you can guess that the pituitary gland is secreting something that's caused a giant to grow too much. So are the individual to grow into someone who's like seven or eight feet tall. By the 1960s, once they have a technology to measure insulin levels, they can now start, and other hormones, they can now start establishing that. For instance, with insulin, the observation was that patients with type 2 diabetes both have high blood sugar and a lot of insulin in their circulation. So they must not be, somehow the insulin must not be working properly. And it takes a long time to establish what that is. You know, is it the insulin that's not working properly? Is it the cells that are responding to the insulin that are not working properly? Like what exactly is insulin therapy? Insulin resistance, excuse me. That takes about a decade just to figure that out. When they have insulin available, this also happens, this is the late 1950s, for the first time ever they have available methods, reliable methods to measure fatty acids in the circulation. And one of the observations was that if you add insulin to fat cells in a Petri dish, in a medium, and you add insulin, then the fat cells will take up the fatty acids in the media. And if you add adrenaline, they will release the fatty acids. And you can do this in, you know, or live mice or humans too, give them adrenaline and take a blood cell when you'll see that fatty acid levels go up. And the way this was interpreted is that, you know, adrenaline is a fight response. So we are presented with a threat, and you start to secrete insulin, and the body, the insulin tells the fat tissue to dump basically stored fat into the circulation, because if you have to either fight or flee, you're going to need a lot of fuel. And you don't want to run out of fuel midway, you know, like 30 yards into your sprint away from the lion, because then, you know, those people who did didn't have any survival advantage, and their children didn't have children. So the realization was was that the hormones are not just there to supply the immediate needs of the body, there's there to supply the anticipatory need. And that includes seasonal needs, for instance, as the seasons change, or if you get pregnant, and, you know, your, your body has to know that there's going to be two people to feed, not just one. The awareness was that the system actually has evolved to take into account the future as well as the present. And you're always balancing the future versus the present. So when you're, then you're trying to maximize both, both the the function of the body and the present, and then, you know, you're maximizing the minimizing the likelihood that you won't have the resources necessary in the future to deal with with the vicissitudes of the environment. Part of the thinking here was that the role of the hypothalamus and all this is that it basically it provides the takes the signals from the environment. from what's happening, you know, do I see prey? Do I see a mate, a potential mate? Is it getting cold out? Are the days getting shorter? And does that mean winter's coming? And then translates those through hormonal and nervous system signals into whatever's nested, whatever functions are necessary to, for instance, store fuel for winter or, you know, make fuel available to the cells like adrenaline does to flee or pump up sex hormone for the mate. Whatever it is, but that's the role that the, that the brain is playing and all that is the intent is taking the observations from the environment and through the central nervous system and through, you know, hormones, endocrine glands in the brain and the brainstem, getting it to prepare for the future for what's happening outside. It's really cool stuff. And it's so absent in any thinking about these disorders. Oh, let me backtrack, by the way, the fat storage for future famines sort of preparing, you know, for the idea is, and again, this was worked out beginning in the 1930s to the 1960s, and then in a field of research known as physiological psychology, as opposed to obesity research, but fat storage is being determined by the central nervous system, primarily an insulin and the hormone insulin. When you consume a meal, you sort of set into play this stimulation of hormones that determine what you'll do with the calories you're consuming. So for instance, it'll prioritize using carbohydrates for fuel because you have no store, meaningful storage for carbohydrates and high blood sugar is high. So if you're eating carbohydrates, you'll stimulate insulin secretion, which will tell the blood, yeah, won't facilitate uptake glucose and keep blood sugar stable and it'll convert some of the glucose at the fat for storage. And it also tells the fat cells to store fat because you want to burn the glucose. You don't want to burn the fat at the moment because you have plenty of storage for fat, but you'll need the fat for the intramural intervals. This isn't just, if you go two weeks without a meal, you better be able to tap into your fat supplies for three days. It's in between meals after, if you're eating a mixed meal, your blood sugar will go up and your insulin will facilitate use of blood sugar for fuel. But as blood sugar comes down, then the way the body's supposed to work, right? Is fat cells see this negative signal of insulin deficiency and they start releasing fatty acids, the bloodstream and your lean tissue and your liver started using the organs started using that fat for fuel. So it's a short term. It's like a wallet more than a bank account. You know, you go to the ATM, you take some money out and you put it in your wallet and you walk around every time you're by, this is, you know, pre Apple pay, you know, you take money out of your wallet and use it to buy meals. And depending on how much you took out in the begin with and how spent for if you are at the end of the day or the end of the week, you got to go back to the ATM and refill the wall and so that fat tissue is kind of like the wallet and the insulin is keeps wallet in your pocket. They supply, so you have to wait for insulin to come down before you use.

Melanie Avalon:
What is the significance, because you talk in the book about how they discovered, I think it's when they were tagging the different fatty acids, maybe with deuterium. I don't know if that was the same tagging situation analyzing, but this idea that it's largely passive, the fat moving in and out of the cells.

Gary Taubes:
It's not so much passing, but it's that it's not necessarily associated with what we're eating or how much we're eating. So, and again, this is, you know, this is a story I tell a little bit in every book, and I'm going to tell more at last, I hope will be my last nutrition.

Melanie Avalon:
your last have you like hit nutrition book fatigue or does it go complete

Gary Taubes:
that it's yeah I mean on some level well first of all you know we've kind of created a revolution so you know before I came along there were you know half a dozen diet books talking about the benefits of low -carb diets and keto like Atkins and feeds with protein power and sugar busters and the zone a little bit crazy as that book was and then you know I sort of my role was to kind of look at all the science and place these books in the in the context of this greater scientific picture that far as I could tell having started off without any bias completely sort of supported the notion that the carbohydrates are the problem in the modern diets and then once my book came out that the end of the world started to explode might have started to explode before then maybe my book was riding a wave rather than causing the wave it's hard to tell now there are dozens and dozens hundreds of books and keto cookbooks and low -carb cookbooks and websites and apps and it's sort of the field is saturated so the only things I really want to write about are I want to have the other confidence that whatever I'm writing is is very probably right and I want it to be you know different well I mean I don't want to write what everyone else is writing and we're running out of anything new to say that's okay and one of the manifestations of that is you see people like first of all you have people advocate for low -carb diets but have to figure out a new way to present them so they're high protein diets or they're low you know linoleic acid diets or they're high satiety diets or anything if you don't have to say what's now become sort of the bedrock approach to successful weight loss and remission of many chronic diseases and then the other you know just a lot of very smart people out there doing this I have you know my approach as a journalist and having become a medical historian at least so far I seem to be better at this than anybody else I've read except maybe my colleague Nina Teichelts

Melanie Avalon:
You know, I had her recently on the show.

Gary Taubes:
It's no fun to write a book that everyone else has written. And then as I say in the diabetes book, I kind of keep unpacking what were chapters in my previous book. So I wrote the case against sugar was a sort of blank unpacking of the science and history of the, you know, 30 or 40 pages I had on sugar and good calories, bad calories, why we get fat focused on the obesity story. And the, um, the dietary implications and the case for keto focused on the dietary implications, primarily in keto story, it was kind of a flip side of the same book, but they were different ways to approach this. And at this point now, I also want to help, you know, people afflicted with these disorders who want to try and fix them to die at the head that think about it the way I correctly. And I've been thinking about this as long and as deeply as anyone around. So I think I have some, uh, uh, the diabetes just was one of these books that had to be read this history had never been covered. There was one quite good history of diabetes disease by a British diabetes specialist named Robert Cattersaw. And I wish he had still been alive or I would have loved to interview him for this book and he did a pretty good job. He never touched diet disease, barely touched that story. And so I felt that had to be written in the last book. I mean, there might be two more books, but it's really getting, um, it's not a lot more blood that could come from the stone, although the last book is also one that has to be read. So.

Melanie Avalon:
I've got one for you that you could write.

Gary Taubes:
Okay, what's that?

Melanie Avalon:
You talk about, I'm joking, but you talk in the book about how there's only three, I guess, fuel sources that could be metabolized by people with diabetes without insulin, which was fructose, fat, and alcohol. You can make the fructose, fat, and alcohol diet without insulin.

Gary Taubes:
It's funny, I mean, that's what prior to the discovery of insulin alcohol was considered often prescribed as part of a healthy diet for diabetes, including for children, because they could metabolize alcohol without needing insulin to do it. Sugar fructose always comes with glucose attached, so even the fructose is metabolized in the gut and then in the liver, most 90 -some huge proportion of it, and so you don't need insulin to metabolize it. It always comes with glucose attached, usually, as sucrose or ifluox corn syrup, and then you have to deal with the insulin secretion from the glucose, and yeah, fat, I mean, one of the... Well, I knew this going into the research for the book that, so what I didn't realize is that through, okay, 1797 is when the sort of first accepted successful treatment of a case of diabetes. So it's a British physician named John Rollo, he's got a patient, he's in the military, he's got a patient, a Colonel Meredith, who comes in having lost a lot of weight, he's hungry, he's thirsty, he's peeing, urine is full of sugar, so Rollo decides that the therapy is that he's having trouble metabolizing carbohydrates because of the sugar and the urine, though it's just coming straight through his body, which is not that accurate, and so he figures a way to treat him is to give him a carbohydrate -free diet, and he prescribes like rancid meat and blood sausages and some grain vegetables, and Rollo gets better, and then he says, okay, you don't have to eat rancid meat, you can just eat fatty meat, and Rollo ends up living for another 12 years, even though he had a pretty advanced case of diabetes when he first appears, and I mean Meredith ends up living for another 12 years. Rollo uses the same therapy for a second patient, a general in the army, and he seems to get better, but then he decides he doesn't want to eat diet, dies like three months later. Rollo writes up these cases in a pamphlet, and he disseminates it throughout the United Kingdom, and he says, you know, to all doctors out there, basically, if you have a case of diabetes, try this animal diet thing and see if it works, and write back to me and let me know. It's like beta testing, a ketogenic diet. This is how successful therapies spread through medicine back before the clinical trial year. You would try it if it worked, or if it seemed to work, you would try it on another patient. If it seemed to work on that patient, you would tell your physician buddies about it, and then they would try it, and so the physicians write back to Rollo, and these pamphlets are published, and nowadays are all available on Google Books, and they said, this thing works. You know, if the patient follows it, they don't, they had all kinds of misconceptions, like if they're curing diabetes, because the symptoms get better, the sugar, the urine is de -sugarized, then why not let the patient go back to eating what they're eating before, because you would cure the disease. This was sort of a common way to approach this always, and you know, an obvious assumption that just happened to be wrong, tragically so. But anyway, through the 19th century, this animal diet becomes a standard of care throughout the world. Then again, physicians, the leading diabetes specialists in the US, the leading physicians in the US, in the UK, in England, France, France, Germany, Italy, Austria, are all using variations on this animal diet to treat their patients. This famous Italian physician, Cantani, is actually locking his patients away for two months, and they can't eat any carbohydrates. And only after they can demonstrate that they can live exclusively on fatty mean green vegetables does he let them out. A famous French physician named Bouchardat, the ad says, look, you know, why don't we put some butter on the broccoli, basically? He said, I don't make it taste better, and it's just a fad. And by 1921, this is actually tested by two physicians at the University of Michigan. They published three articles on it, and the animal was animal's mental medicine, which happens to coexist simultaneously with the discovery of insulin. So by this point, there's a counter hypothesis and a counter theory. And some people are worried about the fat and these animal diets and the reliance of, you know, by the late 19th century, physicians are saying the patients come in emaciated, they've lost a lot of weight. So it makes perfect sense to want to put the weight back on them. So you don't want to underfeed them. You don't want to give them too few calories, but you can't give them carbohydrates, but can give them butter and cream, heavy grain. So let's give them as much butter and cream as we can. And for type two diabetes, they seem to thrive. And then by the early 1920s, there's also a Swedish physician named Petra, who's giving his patients like 95% butter. These are patients with type one diabetes and he says they do better on his effective butter fat diet than they do on insulin. And the German physician Graf, who's one of the leading metabolic disease admissions in Germany, who's written the seminal textbook, Graf in his textbook says, I wouldn't want to live without Petrin's system, but it's hard to get anyone but Swedes to live on cucumbers and butter all day long, but you don't need insulin to metabolize.

Melanie Avalon:
Well, to that point with, you know, not needing insulin for it, it speaks to a ongoing debate. I remember when I first fell into this low -carb keto world and reading so much online debates about this and which is not needing insulin to store fat. And so people would say on low -carb ketogenic diets that fat is a free food, it's unlimited. You can have as much as you want because it doesn't stimulate insulin. Maybe the reason it doesn't stimulate insulin is because it doesn't actually need insulin. So wouldn't that mean fat's not a free food? Like you could just have because presumably then you could gain weight without insulin if you just stored more and more fat. Is fat unlimited on a low -carb ketogenic diet for people?

Gary Taubes:
And the answer is, I don't know, and it's probably depends on individual variation. So you do not need insulin to store fat. And again, you don't want to need insulin to store fat. But what insulin does is it inhibits the release of fat. So it's a hormone enzyme, lipoprotein lipase, that sits on the membranes of cells, breaks down triglycerides into fatty acids so that the fatty acids can get into the cell. And that'll be a sort of passive dissemination through the membrane, for the most part, or at least so I read. You never know if these people got it right, but that's what the story is. Then there's an enzyme in so that fatty acids, I described this in detail in good calories, bad calories, so on and so forth. So you take this triglyceride with three fatty acids and a glycerol and the lipoprotein lipase breaks it down into fatty acids. The fatty acids flow across the cell membrane and then inside the fat cell they're re -esterified into triglycerides. It's kind of a fascinating system because the triglycerides are too big to get out of the fat cell. They won't pass through the membrane. I described this, you know, back when I wrote Why We Get Fat and I used to give lectures on this. I tell this story of when my kids were young. My wife had bought them a, my oldest son's fancy Ikea bed with drawers on the bottom of it and all like this. So I was putting this together on a Sunday in our apartment in New York and I was watching the New York Giants on football while I built the bed in the living room and then I tried to get it into the bedroom and I realized the bed was too big to pass through the door.

Melanie Avalon:
It's the worst.

Gary Taubes:
I had to take it apart, that's what lipoprotein lipase does, and move it through the door and put it back together again, which is basically what happens with the fat cells. And once it's in the fat cell, it's too big to get down, unless you break it down into fatty acids and glycerol again, and the way you do that is with a hormone called hormone -sensitive lipase, and insulin inhibits that. And hormone -sensitive lipase is possibly the most sensitive enzyme in the body to the hormone insulin. So even at very low levels of insulin, insulin is inhibiting the enzyme you need to get fat out of your fat tissue. And again, these are things, you know, people don't get into these kinds of subtlety. I used to try and get obesity researchers, I once proposed this to a guy named Keith Frane at the University of, I forget if it's Cambridge or Oxford, I think it was Oxford. I was in the UK and we got together for a couple hours and we're talking about this. I said, look, keep leading x -ray in the world on fat metabolism, and adipose tissue metabolism. I said, just imagine this, create a theory of obesity from the fat cell's perspective. This is kind of getting back Claude Bernard and the milieu of the cells and all that. The fat cell has no idea how much you're eating an exercise. Okay, it doesn't have any monitor for that. It is connected to the brain and the hypothalamus through the nervous system, so the nervous cell. What those signals do is they stimulate this process of lipolysis, they basically stimulate the breaking down of triglycerides into fatty acids so they can get out of the cell. And then it sees all these things in the cell member in the cell, you know, in the intracellular fluid, the hormones like insulin and glucagon and adrenaline and growth hormone, even sex hormones that all influence fat accumulation. And it sees the amount of glucose and it sees the lipoproteins and all those things. So you can actually create a theory of obesity of a fat cell just based on what it sees and what could stimulate this thing to take up too much fat. But one of the driving forces is insulin inhibiting this process of lipolysis that once it's inhibited the fat can't get out. And that's balanced against the nervous system stimulating lipolysis. So by the mid 1960s, the leading experts on fat metabolism were some really smart people are contemplating that the amount of fat you're carrying in your body is basically a balance of the action of insulin on the fat cell with the action of the nervous system on the fat cell. And if insulin's winning, you're getting fatter and if the nervous system's winning, you're getting thinner. All of that goes away in the science of obesity with this idea that we get fat because we eat too much. And people just stop caring about, you know, I think the way I described it in an essay was we have a science of excess fat accumulation that doesn't take into account the science of fat accumulation itself as though these are two entirely different things. But yes, fat is free, but it's carbohydrates and effective insulin that pretty much determines whether that fat will stay in the fat cells or not, or whether it'll be released, mobilized and used for fuel. And the same hormone that determines fat storage also determine like insulin, for instance, puts fat in fat cells and inhibits the oxidation of fat for fuel. Glucagon does the opposite, not surprisingly. So if a hormone stimulates fat storage, it's going to inhibit fat oxidation elsewhere and the counter -regulatory hormones are going to do the opposite.

Melanie Avalon:
That's really fascinating. I've never thought about that about from the fat cells perspective and what they're actually seeing. So the concept of what the body sees and doesn't sees and going back to that time question about problematic situations now versus the future. You talk in the book about how when we did start having insulin therapy for type one diabetics, that it now was allowing them to live long enough to the point that they would develop these other diseases that the mechanisms of action might have been involved. You can correct me if I'm getting this wrong, but the mechanisms of action that would kill them later probably were active earlier. We just didn't see them because they weren't living long enough for these diseases to actually manifest. And now with this therapy, people are living longer, but they're dying from these problematic conditions. Do you think the body would ever evolve to prevent those long -term disease problems that happen from basically obesity?

Gary Taubes:
I mean, that was always one of the arguments. When you're discussing chronic diseases, heart disease, diabetes cancer, for the most part type 2 diabetes, cancer, you're discussing diseases that for the most part sit in after childbearing age. So the simplest way to think about it is that they're now outside of the range that evolution has any influence on. So yeah, once you've had the child, as long as you're reasonably healthy so you could raise up the, you know, there's no selective advantage anymore from evolution. So that was always seen as a rationale why talking about what our evolutionary appropriate diets might be is irrelevant because we're talking about diseases that, you know, set in late life when evolution, that's probably simplistic. And there are, you know, theories, for instance, that society's that evolution doesn't just have selective advantage on the individual, but it does on the group. And so a population of hunter -gatherers with healthy grandmothers are healthier than not going to have a selection, evolutionary advantage over those that don't have healthy grandmothers. So the grandmothers are also going to now be sold at this umbrella of evolution. It's hard to judge, but one of the problems with all these evolutionary theories, one way or the other, is they're on some level what Kipling would have called just -so stories. You know, why did the camel get its hump? Those kind of things. You're always guessing. You can't test the hypotheses. So there's some assumptions that seem reasonably safe that the sort of low -carb world is based on. And it's funny, the diabetes community, this was another kind of revelation in doing this research. As I said earlier in the 19th century, up until 1914, to be specific, in the U .S. and up until 1921 and the rest of the world, the standard of care for diabetes, the only thing that worked was this sort of animal diet of fatty meat and green vegetables. But there were people who thought that would kill patients. And the counter -argument, this was, you could find this in a half a dozen major diabetes texts, as I did, is that the Inuit and the Gauchos of Argentina all subsisted on diets without carbohydrates. So they proved that humans can tolerate, and they did in two very different environments. And this was an argument for why patients too would be able to not just learn to love it or like it, but they wouldn't kill them prematurely because it was so new to them. And what these physicians didn't really realize and wasn't really a major point of discussion until the mid -20th century was that other things that were new to modern diets were refined grains and sugars and, you know, I'll throw seed oils in, and I don't particularly buy that thinking. And so these new foods, and this was something you could assume is likely to be true, something that's completely new to the environment that we didn't evolve to consume or to do, is likely to do us harm because our bodies haven't had time to adapt to it.

Melanie Avalon:
Something else I wonder, this is super random and out there, but I thought about it while reading your book and I'm thinking about it now. I wonder if, speaking to this evolutionary framework of certain diseases that happen pre -reproductive years and then these other diseases that manifest afterwards, because again, maybe it's oversimplified, but presumably because the body is doing mechanisms to preserve the body up until reproductive years. I wonder if, because we see with like super centenarians that they tend to be pretty healthy up until the certain age and then they just die. So it seems like there's some sort of limit. Maybe it's like the Hay Flick limit or who knows what it is, but it makes me wonder if, say we crack that code and we can unlock the possibility to live past this glass ceiling that we seemingly have on our longevity. I wonder if there'll be a new bracket of diseases that we won't realize once we pass that glass ceiling.

Gary Taubes:
Yeah, hard to imagine that just because, well, again, I mean, it's not on one level. I mean, you know, as things break down, one of the joys of getting older is you realize that things just break, they break on old cars and they break on old people. And if they're external, you know, if their bones and the like can get them fixed, if they're organs, it's a lot more difficult. So I suppose that as, you know, people, more and more people live into their, into their hundred, they'll find unique ways to break that didn't happen before. But I mean, it's interesting, even the center, one of the last magazine articles I wrote before I started doing almost exclusively books was on longevity for discover magazine. And I was interviewing the guys who run these centenarian projects where they study centenarians to see what they do that might explain their, their longevity and the answer I was getting at least circa 2008 or so was that the one thing they had in common was that they had a lot of, they had relatives who had also lived, you know, well into their nineties. And so this clearly seemed to be a protective genes or not necessarily. I mean, some of them smoke, they terrible diets, all of that was kind of irrelevant. What they needed to live that long was to come from a family that lived that long. And then they had a good shot at it. Now, I suppose that means you could identify the genes at some point that made that unique. I remember interestingly enough, one New York researcher said in his cohort that they all seem to have marked, you know, very high levels of HDL cholesterol was one of the few things that stood out, which would be the kind of thing you could get if you eat a very low carb diet, that'll boost your HDL significant life. So maybe there's a relationship, but it's all sort of speculation, my general issue with longevity science is that your, your hypothesis is if I do X, Y and Z, I will live longer and in order to test that hypothesis, you have to do the experiments pretty much for life. Like mortality has to be your end point. And that research, I mean, we do it in mice, but we never know when it mice do has any, can be extrapolated to humans. So it's sort of, do you have a entire burgeoning science that's pretty much outside the realm of science itself because the hypotheses can't be test. And you just never know, like the idea, I mean, we've all gotten used to metform and being this very benign drug, right? That increases, uh, that makes you more insulin sensitive, which would seemingly have to be a good thing, but our a hundred, they're going on a hundred years of experience with metformin is all been in people who eat for the most part standard American or French diets with a lot of carbohydrates in that. So you have no real idea what it would do to someone who like me lives on a, yeah, doesn't eat starches and sweets and grains and legumes. And so burns fat instead of glucose for fuel. Maybe it's not benign for that metabolism. I mean, you really have no idea. So there's an awful lot of guesswork that goes on that ideally we would avoid.

Melanie Avalon:
I get really haunted, especially when I read books like yours, when it's just so saturated in history. I think the thing that stresses me out personally the most is looking back on these historical accounts and what they thought and how certain they might have been at, well, A, two things. Either how certain they were about things that now we know is incorrect and also things they just didn't think about because they didn't know they needed to think about it. You mentioned somewhere in the book how people weren't even really contemplating the mechanisms of fat storage because people weren't really, like they didn't have the obesity epidemic. People weren't really getting fat. And it's kind of like I read a book about the history of fasting and I had the guest on the show and he talked about how for the longest time people didn't, like when people lost weight, it wasn't evident or obvious to them that it was from eating less because they just didn't know. And so it makes me wonder now, and I guess not eating less because we have the whole debate about the hormones and everything, but basically less calories being put into the body than taken out, makes me wonder now things we don't know because we just don't know to think about them. Or maybe, like you were mentioning earlier, we're at this point with AI and all this information that maybe there aren't that many things left that we just don't know that we're not thinking about.

Gary Taubes:
Yeah, it's funny because I'm trying to write an article, an essay. It's in like version 43 at this point for the Atlantic on whether or not the insulin story and the possibility that the insulin story is a cautionary tale for the, the GLP one agonist explosion.

Melanie Avalon:
Once you talk about this, okay.

Gary Taubes:
I keep thinking, maybe I'm just, okay, I'm not a doctor. I'm not, you know, my brain does some things pretty well and other things not well at all. And some things it used to do well. I clearly had too many concussions as a youth and it doesn't do it all anymore. So the insulin story basically, which we started to touch on is you have this drug that is, you know, miracle drug for kids with type 1 diabetes. And because they really are not differentiating enough between type 1 and type 2 diabetes, it ends up being therapy pretty much for everyone who's got diabetes, even the ones who can clearly control it with diet. And because, especially with children back then and still true today, is diagnosis of diabetes was kind of a tragic thing. You didn't want to make the kid's life any worse by telling him he or she now had to eat entirely differently than the other kids, that they can never have chocolate cake ever again or a Coca Cola ever again. So as time went on, the idea was, you know, just let the kids eat carbohydrates, then adults eat carbohydrates, let's just give them enough insulin to cover it. And if that means a lot more insulin, then we'll give them a lot more insulin. And if they start to get fatter, well, we'll give them the insulin, but we'll tell them to watch their calories and exercise. And by the 1930s, as you mentioned, you suddenly start to see this tidal wave of diabetic complications in these patients. So, you know, atherosclerosis, arteriosclerosis, thorotic plaques throughout the arteries of the body, heart disease, strokes, the hypertension, kidney failure, retinopathies, and so they're going blind, no neuropathies, no failure, they're having, you know, lower limbs amputated and these patients who were maybe diagnosed when they were 10 years old, diabetes, and saved from death when they were 12 years old by insulin, like this miracle now, or maybe 27, 30, 35. And they go from being healthy to dead in the course of a year or two. And diabetes community doesn't know what to make of it. And they assume that the problem is poor blood sugar control and not rigorous enough use of insulin therapy. But the only thing they know at this point in time is that the disease is that the, you know, that the kids with the severe diabetes weren't living long enough to see, as you had mentioned earlier, weren't living long enough to see the complicated, to see whether or not they got these complications just from the disease. And now that you're treating with insulin therapy and you're letting them eat carbohydrates, which you didn't let them do prior to insulin therapy, all you could say is that this tidal wave of complications associates with having the disease for 10, 12, 15 years and insulin therapy, using insulin therapy to treat it, and the dietary philosophy, this liberal carbohydrate diet that we're allowing these patients to eat, and we're allowing them to cover it with insulin. And any one of those, or all three of them, could be causing the complications, but they have no way to tell. This is no way to determine, they believe so strongly in insulin therapy, they just sort of reject any possibility that it could be that, and yet it clearly could be. And today that question is unsettled, you know, a century after insulin therapy. It could clearly be the diet. So if they never let them eat carbs and minimize drug use, insulin therapy, which is basically what Richard Bernstein began at, hating on Bernstein's diabetes solution, 1980s. If they just do that, they seem to thrive, so it could really be the diet, and they just couldn't tell, nobody could tell. And so, again, this is the philosophy that carries forward ever since. But one of the issues in trying to figure this out for the sort of present and the future, you mentioned the certainty with which people say things, you know, in interviews, and then the only thing I know for certain is how little people know, so the likelihood that they still know very little. And with GLP1 agonist getting back to the story I'm trying to write for the Atlantic, it's clearly in its own way a miracle drug. I mean, people who struggle with obesity their whole life for whom it's an intractable disorder can suddenly lose a significant portion of their excess weight. That's a wonderful thing. And for adolescents in childhood, just as type 1 diabetes is, you know, terrible disease and fatal obesity in childhood and adolescence can be a pretty terrible disease too, even if it's, you know, just a chronic disorder or not, by no means fatal. And so you've got this wonder drug and you see people embracing it and suddenly diet becomes secondary or tertiary. Now we can really pay lip service to diet because we got a drug. And you could easily see a situation 20 years from now where we've completely misunderstood the cause of obesity and how to prevent it and how to treat it because of the introduction of such a successful drug. And you could also see a situation where just as many of the complications of living with diabetes for years to decades could be caused by the insulin therapy, it's quite possible that over years or decades of the use of GLP1s, and the younger you are when you start the longer you'll have for this to happen could be caused by the drugs or exacerbated by the drugs. And it'll be very hard to tell, you know, it'll be hard even to do an observational study because the people you would have to compare with your controls would be patients who never went on the drugs and maybe never lost any weight. And so also died prematurely, but just from the complications of the condition, not of the complications of the condition and the therapy, or and the therapy in the absence of any dietary therapy. So there are a lot of real parallels that are a little bit scary while simultaneously recognizing that these drugs are fairly remarkable and, you know, I can understand the appeal.

Melanie Avalon:
Sounds like the beginning. It's either the beginning of a horror movie or of a, I don't know, like Lord of the Rings, like a victory.

Gary Taubes:
No, it's funny, I say that in the article where, to one point, you know, talking about, I mean, again, the long term, what happens, so we study the, we, the pharmaceutical company, the medical, the obesity research, have studied what happens if you go off these medications after a year or two. But what happens if you are on them for 20 years and have to discontinue? And can you discontinue? And so let's say after 20 years, your body is habituated to the drugs that are no longer really working. You've gained the weight back anyway, and now you are having side effects that make them intolerable, but maybe you try to get off and the side effects get worse, not better. This is a pattern that happens with existing drugs, benzodiazepines.

Melanie Avalon:
This is everywhere, this pattern.

Gary Taubes:
And I think in the article, whether it was this, I say, you know, we have no idea what will happen when people try to do this, but at the risk of sounding ominous, we will find out.

Melanie Avalon:
What do you think is the role of science and medicine making those judgment calls? Because you were talking about how with the kids on the insulin that basically it was that it would be too difficult for these kids not to eat the carbs, so we'll just cover it with the insulin. There seems to be this idea, and you talk about it a lot in the book, basically weighing the potential physical issues of disease or future disease with the psychological or the stress burden of sticking to a diet that might be, you know, seemingly difficult to stick to.

Gary Taubes:
So that's what, you know, you could, what a thought experiment. So let's assume that would Bernstein has observed with himself. So Richard Bernstein diagnosed with diabetes in 1946 at age 12. Like by 1970, he's got a degree from Columbia university and then in physics. He's working as an engineer. He's doing the best he can to keep his diabetes under control. And yet the complications are setting in. He's got all kinds of problems, including hypoglycemia that sends him to the hospital roughly once a month. And he decides he's got to do something about it. And he buys, uh, comes the first person ever to buy a device that allows him to measure his own blood sugar at home, literally patient number one to do this. And over the course of about three years, he does a series, got an engineer's mind, so he does a series of studies and he realizes that he can essentially keep normal blood sugar, like the blood sugar of a healthy human being, a healthy non -diabetic, if he avoids carbohydrates entirely, and then he can use very low doses of insulin because of the law of small numbers. So, you know, no carbs, low doses that minimizes the mistakes. It minimizes the variations. It minimizes the response of your body to what you're putting in it and what you're injecting into it. And to make a long story short, he motivates the medical community to study it. He prompts the use basically of, of home glucose monitoring. He gets as much credit as any human being alive should. And then he writes books, goes back to med school in his forties, the oldest medical student ever at Einstein, and gets his recommendations written by the leading diabetes specialists of that era of the 1970s. And he writes his books and he becomes a doctor and treats diabetes. And he's still alive. I think he's turning 90 in May and he's still practicing. Did you interview him? Yes, yes. I, we spend holidays with my in -laws about 10 miles from where he lives in Westchester County. So I spent about six hours with Richard Bernstein. Didn't mean by the way, he's a cantankerous guy. I have no idea if he liked my book. No, you know, I basically say, give him complete credit for catalyzing a revolution and diabetes therapy that, you know, in other worlds would have won. If he had been a physician, I would have won my Nobel prize or a academic researcher. Anyway, if that's true. So let's say if in 1921, when insulin is discovered, if these people and leading diabetes specialists time, a guy named Elliot Jocelyn, his clinic in Boston, he had the first dedicated diabetes clinic in the United States. And that became eventually the Jocelyn Diabetes Center, which is associated with Harvard, Jocelyn argued at the time for very low doses of insulin and then the very restricted diet as the safest way to approach using this drug. But he was pretty much eventually just outvoted by people who said, look, the patients are going to stay in a diet anyway. And then like I said, by the 1930s, you have this tidal wave of complications. Imagine if in 1921, they said, look, you can do this. You can do this Bernstein's protocol. So you're not going to eat grains and starches and rice anymore, but we're going to minimize your doses of insulin. And, you know, Bernstein never really got into ketogenic diets because he kind of believed the saturated fat story when he was doing this. It was so well accepted, but you know, you could eat a high fat, high, pretty high calorie diet, just don't eat these foods and you'll be healthy or you could do what we are going to do in 15, 20 years from now, you're going to suffer this tidal wave of complications and go blind and have amputations and die. It sounds like a crazy way to describe it, but that appears a hundred years later to be a valid description of the options. And now, of course, we have much better drug therapy and much better drug delivery devices like insulin pumps. We have them, you know, so you can delay all those complications instead of 10 or 15 years. You can now probably go up 40 years, but people, you know, if you do the opposite, with type one, Bernstein's method and type two is effectively a ketogenic diet, this animal diet circa 2024, it looks like it could put the disease kind of into remission and not suffer the symptoms. I mean, even Bernstein is alive at 90. He spent the first 24 years or excuse me, 16 years, 18 years with the disease pretty much uncontrolled. So a lot of the damage he suffered, a lot of his issues might have been backed off by the poor control in the first 18 years. They didn't know enough to think like that or to do that. And today when they should, it's hard to announce all those belief systems and step outside of it. That's why you need somebody like a journalist like me who's outside the system, because I could come along and say, look, I'm not wedded to anything you've done so far. I just want to find out why we have such, you know, why in 2024, 40 million Americans have diabetes as opposed to like one million, one and a half million in 1960. And why it's still considered a chronic progressive disease and multiple drug therapy is the norm and people have to deal with the complications of these drugs. That doesn't have to be the case. You know, the evidence today is this does not have to be a chronic progressive disease. This disease can be put in remission by diet. So, shouldn't physicians and patients know that and advocate for it? Say to their patients, when diagnosed, look, you could do it this way. You know, you could pull the diet lever and you won't even really know you have the disease, but you're not going to eat a donut again or drink a Coca -Cola or eat pasta, okay? Or you could do the drug thing and then you could have all the donuts and Coca -Cola you want, but not all of it, you know, moderation. And you'll get fatter and you'll get this, well, GLP ones will solve the getting fatter problem. But you see the point. There's sort of two ways to look at it, the traditional way where we know it's a chronic progressive disease and the dietary way where it does not appear to be. And where you can put the disease into remission, can we offer that? There's a viable possibility.

Melanie Avalon:
Maybe a marriage of the two ideas would be if the system could prescribe a pill that the pill, it would just be a sugar. Well, no, it would not be a sugar pill. It would be a pill. I don't know what would be in it. Something completely benign and it would have a lot of instructions. Like you take this pill, but this pill cannot be taken with sugar or carbs or like turned into a pill system, but you have to make dietary changes to take the pill.

Gary Taubes:
Well, it's funny because the GLP1 agonists or Gobi and asymptomatic and all those may do that to some expense. People talk about their, their, their, their appetite's completely inhibited, but I haven't heard yet like for what? Like for sweets, for beaker, for prime rib, for, is it macronutrient specific or is it all foods? The other thing I once I was approached by a Wall Street guy who had developed a pill that you suck on, it dissolves. And then for the next two hours, carbohydrates don't taste good and sugar tastes off for you. So as a sort of something you couldn't take before eating to target your carbohydrate consumption and it worked. But what I noticed was I had to make the conscious effort to do it before eating and I didn't want to do that. If I knew I was going to have something sweet or wanted to have something sweet. It's like, I didn't want to shut that off. Yeah. I might end up with a sort of more primitive perspective, which it looked, you know, if we just, actually, let me tell you one other anecdote, which is one way to think about this. And this was told to me by, um, and it's in the book in the epilogue, uh, a chef turned journalist who was diagnosed with type one diabetes in his thirties. This was back in 2016. And when you're diagnosed with type one diabetes, you're in effect dropped into disease land. Like here's a disease you may never have thought of about before, unless one of your relatives or friends has it. And suddenly you're told you have it and it's a serious disease. You have to learn as much about it as you can in a very short period of time. And your physicians and your diabetes educator, maybe your endocrinologists are going to do their best before they even let you leave the hospital to teach you how to inject insulin and, you know, what it feels like to have a hypoglycemic episode and how to deal with that with the necessary sugar pills or whatever. And, and so the doctor was explaining to this young man, what young by my standards, you know, that he now has a disease in which he can no longer tolerate the carbohydrate content that diet can metabolize them safely. And the reason is he's, his pancreas is no longer secreting enough insulin to do that. So they're going to give them insulin and then they're going to have them eat a set amount of carbohydrates at every meal for the insulin cover. And he says to the doctor, so wait a minute, let me get this straight. What you're telling me is carbohydrates are now poison to me and insulin is the antidote and I should eat the poison and take the antidote and in fact, eat enough of the poison to make sure the antidote doesn't kill me. Why don't I just not eat the poison? We'll need the ant. And it's like the doctor was mystified by this logic because he never really thought about it before. And the doctor assumed that he would never be able to stick to a diet. And because it's basically, if I'm not eating the carbs, that's it for all intensive purposes, ketogenic diet. And we know that nobody sticks to it. This guy actually says to his doctor, I don't understand if I, you want me to exercise, if I said, I'm going to go work out two hours a day, five days a week, you wouldn't tell me, well, no one complies with that kind of exercise program. You would say, Bravo, go for it. But if I tell you I'm just not going to eat carbohydrates, now you're going to tell me I can't do it in advance. Why not? Let me try. And so it's sort of the medical community that we, and this I've described in my other books, they created all these thought processes. They, they miss these very obvious ways to deal with these diseases. You can't metabolize carbohydrates safely. Don't eat them. You don't need them. We don't have any physiological requirement for carbohydrates like we do for fats and protein. We know, as the 19th century doctor said from the, the Inuit and the, the gauchos of Argentina that you can thrive without these foods in your diet. So just don't eat them. And then we can minimize your drug use. If you have type two, you probably won't need any drugs at all. If you have type one will minimize your insulin, which will minimize swings in your blood sugar, which will keep your blood sugar stable, which is the goal. And they just had all these excuses, rationales that they had developed in their misconceptions over the years so that they couldn't, wouldn't take seriously the most obvious approach to treating this disease in a way that would keep the patient the healthiest, even if it meant the patient had to make some sacrifices, which they would anyway. These would just be sacrifices that actually worked.

Melanie Avalon:
So crazy and not to keep on with the really the dark train of it all but it's really interesting with something like cancer for example and chemotherapy which has a you know as miserable to go through and a lot of terrible side effects but they don't make that judgment call there like they don't say chemotherapy is too hard for you so we're not gonna offer it. I find it really interesting like where they make the judgment calls about what we as humans can and cannot

Gary Taubes:
do. But funny, I used that exact same metaphor just last week. So a very good friend of mine was diagnosed with Parkinson's. So she's 68 and her husband is a very good friend of mine. I was talking to him about and I said, you know, there's some anecdotal evidence that ketogenic diets can inhibit the progression of Parkinson's and maybe, you know, at some level help minimize symptoms and they say, yeah, that's a lot of trouble and, you know, my wife is, she's going to be, she really likes her, her carbs and her wine. And I said, look, if she was diagnosed with cancer, right, and doctor said, we're going to be on a chemotherapy program for the next six months, she's going to feel, you wouldn't say, well, she's going to feel miserable, I'm not going to do it. You would say, okay, you're going to feel miserable, you're going to have to do it anyway and hopefully at the end of six months, we'll have solved much of the problem with disease and then you'll feel a lot better and we'll go from there. So why not think the same way about ketogenic diet? First of all, I don't think she'll be miserable, even if she misses her wine and her pasta, but give it four months, do it right and see if she feels better and treat it like chemo therapy. It's like, look, we're just going to do this, we're going to go, we're going to show up every meal. Let's see if you feel better. And if you do, then after the end of four months, you'll know what your balance and what the trade off is, is it really worth eating my pasta and my donuts and having my wine and suffering this slow progression of this disease into, you know, premature death or do I like being healthy, relatively healthy, more than I like eating a donut. So you know, we'll see how that goes.

Melanie Avalon:
So, so crazy. This has been beyond amazing listeners and we didn't even remotely touch on. There's just so much in your book. I just can't even I mean, we didn't there's so many, so many little things like we didn't talk about like how they use insulin to treat schizophrenia, which was pretty mind blowing or like all these other different options that tried and actually did sort of work that weren't low carb like the oatmeal diet or the sugar cure. Basically, there's a lot of really interesting things in this book. I highly recommend everybody get it now. Rethinking diabetes. Thank you so much, Gary. And you were saying earlier that you didn't, you know, you don't know if you were causing the wave or riding the wave with, you know, your initial work. And I would definitely vote for even if the waves were already there, like you definitely catalyzed everything and created the tidal waves with all of the work that you were doing. And I just can't thank you enough. And I can't wait for your next maybe last book. Do you anticipate when that will be coming out?

Gary Taubes:
I would have said, say maybe January, 2026, but I put things on hold for a while to work on this sub -stack in Taisho. So we're doing a sub -stack together called Unsettled Science, regular articles and essays and criticisms of the work coming out, nutrition and chronic disease science. And so I'm trying to get that up and going. I mean, and I see it as we're kind of in startup mode, so we have to work on that too much to get to the point that it's actually generating an income, we can cut back and go to the other things that interest us in life. So my obesity book might be delayed by about six months. It's basically a, it's very, it'll be like rethinking diabetes and that it's going to be history of the science of obesity, which has never really been written. And again, it's on some level, I discuss this in every one of my books, but this idea that obesity is, it's a fat storage disorder, it's an energy balance disorder, it's not about eating too much and how that theory arose and why it arose and what happened to it. And when I first started writing about this for good calories, bad calories, I had maybe, I don't know, I had a lot of German and Austrian writing. I mean, they were doing the major research on fat storage and on fat tissue and obesity up until the second world war. And I had only the stuff that was translated into English. Now I could get all the original, not all the most, let's say 80% of the original documents and can get them translated by AI programs. So it's just opened up a whole new world of fascinating, really smart people talking about the same subjects that are controversial today. And on one level, I can't wait to write it and do it. And on the other, it's like, I got to get the sub stack going. So trade off.

Melanie Avalon:
That explains why, okay, so, because I went to your sub stack, because once I had Nina on the show, I immediately subscribed to her sub stack. So then I went to your link for the sub stack and it pulled up Nina's and I was like, wait, where's Gary's? Okay, that makes sense now. Okay, I got it.

Gary Taubes:
Yeah, well, in theory, it's both of ours. We're still working on, because it was Nina's first and I joined her, there are still ways, like if you Google unsettled science, it'll say unsettled science, Nina, Tyshult, Substack, it's both of us. And we're still trying to figure out all the ways to sort of have it, you know, make it clear that it's both of us.

Melanie Avalon:
Did I tell you when I first wrote my book with a traditional publisher for stores what they said about you?

Gary Taubes:
And I didn't know you didn't, but...

Melanie Avalon:
Okay, so because I originally self -published my book and then I got my agent and we were rewriting the book to publish and the legal department, was it the legal department or the editor? I guess it was the editor. They actually didn't have that many comments about things they wanted me to change. There was a big red sticker on your name because I had talked all about what I learned from your book and they were like, you have to put some sort of disclaimer here about him. I was like, what? And they were like, yeah. So I went in, I'll have to show you what I ended up writing, but I put something that I was happy about. It basically put in a disclaimer sentence about how your work was debated among people. And then I just kept everything I said originally, but I thought that was really funny.

Gary Taubes:
And it's funny, I was one of the sub stacks I recently wrote and the way we've been doing it as one of us to write in the other one, you know, we'll edit it. I had said that there was a meeting in Copenhagen, Novo Nordisk, the company that makes the GLP one agonist, their foundation had invite only meeting of old expert obesity researchers. And I put the word expert in parenthesis and quotation marks. And then I had a parenthetical saying, I put experts in quotation marks because I was included in the group. And I was, you know, basically Dana was like, this is crazy fake humility, Gary. It's like, of course you're an expert. And it's like, well, maybe an expert to us, but 95% of the relevant medical community thinks we are wrong and I am not an expert to them. And I would like to acknowledge that. I think I, we took it out, but it's sort of, I might have, you know, it's a difficult, the problem with, and I have to, I do want to write a sub stack about this, just challenging the conventional wisdom, often when people report about my work, the way they'll do it is I want to view me and then they'll find like three people who have never read my books to, but I have prestigious appointments who will explain why I'm a quack. And I always want to say to them, you know, people who haven't read my work to saying I'm a quack is meaningless because because I'm challenging their work, they have to think I'm a quack and I have to think I'm wrong because I'm saying, look, this journalist thinks he knows better than you do what's and what you should find. And I could give you the names are the people who have these respected, impressive appointments who have read my book and think I'm likely right. They're the meaningful ones because they've, you know, they actually went through the trouble to try and assess my arguments, not the ones who just know I'm wrong because I disagree with them. That's crazy.

Melanie Avalon:
I know you have to go. The last question I usually ask is just what's something that you're grateful for so we can end on a happy note.

Gary Taubes:
everything. My oldest son got into a good college, which means we haven't screwed up his parents yet. Or at least not noticeably.

Melanie Avalon:
Well, thank you, Gary.

Gary Taubes:
Thank you, Melanie. This was really, I had a lot of fun. So thanks.

Melanie Avalon:
Awesome, I did too. Have a good evening.

Gary Taubes:
Okay, you two, take care.