How Carbs RUIN Your Health and Biomarkers! | Stephen Thomas

In this episode of the Plant Free MD podcast, Dr. Anthony Chaffee interviews Coach Stephen, an experienced personal trainer and health coach from the UK, who details his journey from advocating high-carb diets to embracing and teaching low-carb, ketogenic, and carnivore diets. Stephen recounts his early life following conventional food guidelines, which he now believes contributed to his mother’s colon cancer and his own health decline by age 50. His turning point came after observing superior health outcomes in patients ignoring mainstream dietary advice, particularly those reducing carbohydrates or following what would now be called a carnivore diet.

Stephen describes the benefits he and his clients have witnessed from adopting low-carb or carnivore diets. He emphasizes the reversal of type 2 diabetes, improvements in kidney function, and reduction of chronic pain and other “irreversible” conditions. He notes that many medical guidelines and lab reference ranges fail to account for physiological changes that occur on these diets, leading to misinterpretations, especially regarding markers like HbA1c, thyroid hormones, and insulin levels. Stephen believes current standards are often based on averages from populations with mostly high-carbohydrate intake and thus are not optimal references for those on low-carb diets.

The discussion delves into the limitations of certain blood markers and lab ranges. Both Chaffee and Stephen argue that markers such as HbA1c can be misleading in low-carb populations because of longer red blood cell lifespan and other physiological adaptations. They explain that clinical health and how patients feel are more important than solely focusing on lab numbers. They caution against “gaming the system” to hit conventional targets, which may not reflect actual health improvements and can sometimes be detrimental, such as pushing for higher insulin or T3 just to fit reference ranges.

Stephen and Dr. Chaffee also address concerns over “insulin suppression,” thyroid function, cortisol, and other hormonal adaptations on low-carb or carnivore diets. They assert that low levels of insulin or thyroid hormones often simply reflect the body’s reduced need for these hormones when not consuming many carbohydrates—not a pathological state. Citing clinical and historical evidence, they argue that carnivore and ketogenic diets can restore metabolic health even in challenging scenarios like type 1 diabetes, thyroid dysfunction, and iron overload.

The episode concludes with practical advice: focus on species-appropriate diets (fatty meat and water), listen to one’s own health signals, and avoid getting too concerned with lab values that don’t match clinical reality. Stephen encourages listeners to learn how to interpret their own blood work in the context of their diets, to utilize resources like his Substack, and to participate in supportive communities. Both guests advocate for using real-world health outcomes over chasing arbitrary numbers, and stress that long-term dietary consistency and patience are keys to sustainable health improvements.

Coming soon…
[Music] Hello everyone. Thank you for joining me for another episode of the Plant Freem podcast. I’m your host Dr. Anthony Chaffy and today I have a very special guest, good friend of mine, Coach Stephen, all the way from the UK. Sunny old England. How you doing, Stephen? Yeah. Well, you’ve hit the day when it’s sunny today. Yeah. Yeah. One day of a year. Yeah, summer is here. You know, it’s good for this afternoon. There was the um with that Little Britain, that little sketch comedy show. They’re talking about, you know, summer in um summer in Scotland is is on, you know, September 14th between 2:15 p.m. and 2:35 p.m. and things like that. It was this wonderful time this year. Get outside, look at, oh, this is great. And then it just starts raining again. They go back inside. Yeah. Yeah. That’s sort of how I felt when I was over there. Yeah, that’s it’s true. If the sun comes out, we report it as a UFO. So, yeah, there’s that, too. Well, that’s good. Um, well, so Stephen, for people that haven’t uh come across you before or don’t know you, can you tell us a bit about you about yourself and and what you do? Right. I’m 61 right now. And, um, for many, many years, I was a high carb advocate, an advanced personal trainer, and um, I really thought I knew it all. I did a bodybuilding show. I won a tennis tournament, semi-pro soccer player, so I was pretty fit, not being bigheaded, just giving people some context. And um I mean, we spoke just before we came on. I’d lost my parents very early in life. And the reason I mentioned that is because my mother died of colon cancer. I was only 23 and both my mom and my dad believed the food guidelines and followed the food guidelines. And sadly um my mother was a product of eating lots of fiber because as her colon got worse they just prescribed more and more fiber um things like ensure as well complain and all these high sugary drinks and she just plummeted. She didn’t have any particular affinity to any any particular food group or group. She just followed the guidelines. And so I did. And I I suppose it’s one of the things I always go on about when people talk about genetics. No, you eat what your parents eat in the main when you’re a kid growing up, which is why I’ve got not just English teeth, but really bad English teeth. Um I avoided red meat, saturated fat. And the point being up until my 40s, I thought I was doing the right thing. And then um I’ve got two honors degrees in my life. One is in English literature, the other is physiology and health sciences. And um I got to the stage where I was really lucky to train an athlete who had type 1 diabetes. And this is my mid-40s and uh obviously she wasn’t. And we got her to the Olympics. But what that triggered in me was an interest in the fact that she knew type 1 diabetes better than anyone I’d ever met or been trained uh trained about. And um she didn’t follow any of the guidelines. She did what she thought was best for her, which was great. And it was nice that she employed me to train her. So, I was about 45 at this point. And maybe I should have realized that everything I’ve been taught was rubbish, but I didn’t. And um we were doing a lot of lab testing and I got involved in that as well. And you know me, so you know where this is all converging, I would imagine. Anyway, um I started to think, well, this is this is strange, but maybe it’s a one-off because he’s type 1 diabetic. that’s very different to everything else. And I really got interested in um helping people lose weight and try to manage diabetes full stop. So I started a clinic and I um got qualified as a specialist practitioner, not a general practitioner in obesity and diabetes. And this is where it took a really funny turn and I kick myself when I look back. But I used to take in groups of 10 people and we’d follow them over a few weeks and then there would always be a new group. So there’s always a cycle of new people and the ones that invariably did well when I asked them what are you doing? They said ignoring you because they they were they were basically um doing what we would now call carnivore but they called it Atkins or they were doing keto which we which you know at that point they just said we’re cutting out carbohydrates. It took me four or five years to really wake up and also we were doing blood tests. We were getting uh you know nurse practitioner in and I noticed that the bloods the results and what the doctor’s comments were who hadn’t seen these people didn’t make any sense compared to the people. So we had these these bloods coming in a doctor’s comments from sort of a a remote area and uh you know I talked to the person and say well you know they’re really destroying you here but you’re one of my success stories I don’t get this. So I trained in phabbotomy as well. So come uh age 50 I realized that I’d got it all wrong. I’d been lied to and my own health had taken a really bad turn. I had a coronary artery calcium scan of 639. Didn’t smoke, didn’t drink, didn’t have red meat, didn’t have saturated fat. I did all the things. Uh here’s a kicker. Um I had lower left quadrant pain. Had a colonoscopy. I mean you work in a clinical setting. I can remember sitting in the outpatients bit genuinely thinking that’s it. I’m going to die because my mom had colon cancer. It’s all genetics. I I’ve got a pain in the same area. Here I am. My heart shot to pieces. My lower left quadrant is um giving me lots of pain. My blood told me I was, you know, becoming diabetic. It was all going wrong at 50. And um of course it didn’t. Here I am 11 years later and what changed it? taking out the carbs, not listening to the food guidelines and listening to the people around me and using my eyes and my ears and my brain and thinking none of this makes any sense. And um you know when I did the diabetic training I was really cross with the fact that none of the doctors, none of the physicians, none of the training staff wanted patients to have glucose monitors in their hands because they said, “Well, if they have that, they won’t listen to us. they’ll do what, you know, is literally saying they’ll do what’s best for them. Um, which is really stuck with me because this isn’t a, you know, a rant against the medical people. It’s it’s about the medical system. You know, there are no nefarious people working in these places. They genuinely believe what they’re taught. So, it’s it’s really top top down. That’s that that’s the problem. Right at the very top, the guidelines and uh, you know, big farmer, big food and all that. Anyway, the point being went low carb. That worked okay. Did keto up until about age 55 and then um joined me RX with Shan Baker. Mhm. Got into carnivore. Um I used to do his Thursday diabetes meeting which was you know hats off to Sean for having a faith for me to let me do that. So that was really good. Then went out on my own. Um did a bit of the steak and butter gang. Yeah. hooked up with Richard Smith do live question and answers on YouTube from State Control Britain every Sunday at 7 p.m. And um yeah, we got more and more qualified in every area really. And um I haven’t been to the doctor for 10 years. I’m not on medications. I’m not diabetic. Um my lower left quadrant pain disappeared. My athletes foot went uh all naturally. So basically um to quote you just eating meat and fat and drinking water and doing all the things that are species appropriate literally changed my life. That’s great. And um now you’re you know preaching the gospel you know and bringing that on to other people which is great too. Um so is that is that um so what are what is your main focus on your work now? Is it are you working one-on-one with people, working in groups, or trying to just make content to try to get this out to as many people as possible? Well, that’s great uh question because it’s a bit of everything. So, I do onetoone consults online. Um Richard Smith, uh the keto pro and myself, we run a school group, school community. So, that we do meetings three times a week. So, that’s sort of groups of like 40 people. And then we do our live question and answers on a Sunday which is about 2,000 people. But I also write a Substack which is a daily article based on uh my experience labs. I teach people how to interpret labs for themselves because going back to that thing about putting the glucose monitors in people’s hands. I want to put the knowledge in people’s heads. So I don’t I try to demystify it all. Break down terms and that gets about 80,000 people reading every week. Sorry, every month. I like it every week, but yes, every month. But I think that’s um that’s it. I think you’re the you’re the same. You play out your audio podcast. You go you do uh you know public events. I do that as well. And I think just get the message out to as many people as you can in in different forms. So I’m on Spotify, YouTube, and like I say, Substack and doing live Q&A and all that. So yes, get get it out every way you can and actually meeting people face to face is really great. So when we do the meetups, that’s that’s really good. Very good. And then so obviously you’ve started applying this out to other people. And um the reason that I do this is because I’ve just seen so many people benefit from it. I mean, I my, you know, my happy place is in the O. If I could just operate all day every day and that’s it. That that’s where I’d be. Um, but it’s something that I’ve actually, you know, put to the side for a while because I just I it’s this just helps too many people from what I see. And so that’s I’ve sort of changed my practice to that and helping people online as well. But in your experience, what have you seen um carnivore diet or even just low carb, you know, therapeutic carbohydrate restriction, ketogenic diets, what have you seen this improve in people’s health outcomes that, you know, typically we’re we’re still thinking are irreversible sort of conditions? Uh well, I suppose the most striking uh amount wise is reversal of type two diabetes. And maybe that’s because of my background. So I attract that sort of person in in the first place and that you know that’s the way it is. If you specialize in back pain all you see is people with back pain. So uh that’s your world that’s your bubble. So I think reversing type 2 diabetes is is probably top top amongst things but some really strange things that seem to have become a bit of a niche like uh returning kidney function. Mhm. But that isn’t that odd when you know the joined up thinking because if you can most people with kidney function problems have a glucose um intolerance problem or they are already diagnosed as diabetic. So you literally say if we fix your um glucose intolerance we’re going to fix your kidney by sort of default. And this isn’t just minimal stuff. I mean I’ve literally had people that have come in and one in particular was given two weeks to live. So the kidney function is really low. Yeah, absolutely. So we’ve reversed a lot of um kidney function problems. Got it, you know, getting the filtration rate up, the numbers up. Part of that is down, you know, to the misinterpretation of the EGFR, which is an estimated glus filtration rate um which is based on dietary protein intake or creatinine or the waste of that particular way of eating. So getting people to have a cystin C which is not relying on dietary protein. Mhm. To to firstly get a really good baseline number because you could magically say um I am going to fix you. You know do two weeks of this thing get a cyst in C and and why lo and behold you’ve improved the numbers by a lot. Um I’m alluding to something else there. Messing with the numbers is not what I want to do. I want to get people fitter and healthier. So once we get a baseline that’s bit more reliable which is the cystatency then go from there and um but even that has push back from the medical fraternity that wants to stick with EGFR which is unreliable luckily and it’s the only good thing to come out of wokeism is uh in 2021 a big group said that the EGFR is racist. That’s because it you know because the calculation has a you know has a racist factor to it. So if you’re from a certain ethnic background, they will take your number and multiply it up by 1.6. So um uh that’s the only good thing to come out of wokeism. So I I think that’s quite interesting that they want the cyst as well because it takes that out as well which proves it’s a it’s a much better number. So it’s kidney function probably it’s the second one and I I would then be very wide and just say just general overall health it you know many people come and say I didn’t realize that that the joint pain I had wasn’t age it was the way I was eating so they might come for a particular reason and we use diabetes as that reason but then they will say maybe six weeks into this wow I didn’t real I can go down the stairs now without you and my knees are hurting. Um or their skin will clear up, something will happen which they didn’t even realize. So when we’re in the school community, only last night had a guy saying, “I’ve just realized that my ankle pain’s gone.” Mhm. But the absence of a pain is is a is a really weird thing, you know, because if you have a bad shoulder, it just bothers you, bothers you. If you wake up one morning, it’s gone. And you’ve got a busy day, you might just go through the day not even realize. until someone says, “Is your shoulder still hurt?” And you go, “Oh, no, it isn’t actually.” So, I think there’s a lot of undiscovered illnesses out there. People don’t realize and they’re accepting, which is what I did when I was 50 and sat in that room. I thought, “Oh, it’s all genetics,” which it isn’t, by the way. Um, you know, it’s it’s more epigenetics, much more epigenetics than we believe. Um, so the way they start eating and eating species appropriate diet and to steal Kenber’s thunder, you know, the proper human diet, um, can cure things you didn’t even know were wrong with you. Yeah. Yeah. Absolutely. And I’ve seen that with cyatin C. I’ve seen people with, you know, endstage CKD. I mean, bordering on needing to go on dialysis, uh, being able to to actually reverse it on a dime. And a good friend of mine actually was down to like something like 19% uh kidney function. And um he then switched and his his his doctor said that, “Oh, you’re going to kill yourself. That’s going to destroy your kidneys.” And he just said, “Look, everything you’ve been telling me, everything you’ve been giving me has just made my kidney function get worse and worse and worse until I’m I’m, you know, bordering on needing to go on diialysis at 35.” And um so I’m just going to try this. And within 3 months, he had increased up to 80% kidney function. And his uh nefologist kept saying like, “You got to stop. You got to stop. This is going to kill. This is going to kill your kidneys.” It’s like, “What what lab test are you looking at that that I’m not seeing here.” You know, it’s like the stuff that you were doing was making making him worse and the stuff that uh he was doing um obviously reverse that. But I’ve seen that too with cyat and C as well. I had um um a lady uh who came up to me at a conference and she said that her husband was again in that in that area of almost needing to go on dialysis and um they were both physicians and they gave this a try and all of a sudden it just sort of it turned the ship and his his creatin you know to your point the creatinine didn’t really change but when they checked his satin C that started improving and getting a lot better and so so his you know estimated filtration rate via the catatin C that started improving and going up as well and he’s clinically doing a lot better as well. So that’s that’s definitely something I’ve seen before also and you know and and at other times too I’ve seen people’s creatinine come straight down as well. So that you know the traditional ways of studying the EGFR I’ve seen that improve as well but anybody who is sort of stagnant or a bit high just remember that I mean even people that have a lot of muscle mass and things like that will tend to have higher cyatency or sorry higher creatinine levels and and therefore lower EGFRs. Um but yeah and um you know you you mentioned that about you know gaming the numbers and just trying to trying to get an effect um based on a piece of paper and as we were talking about before we came on there’s a saying in medicine which is you treat patients you don’t treat lab tests and um and so but sometimes this is all they go on they just go on like well we need we need this number or this number range and I mentioned my patients that um had um they needed to take a cholesterol test for like an insurance test or something like that. And so what they did was they understood the physiology because we spoke about this that when you go on a ketogenic diet, your LDL and HDL go up because LDL and HDL transport fat around your body, fat, cholesterol, and proteins from your adapost tissue to your liver. And um and so if you’re running on fat, you you need you’re running on more fat, you’re going to need more LDL and HDL to transport that fat. It’s pretty straightforward concept. And also, you’re getting rid of these plant oils that have um that have these plant steriles, the plant cholesterol that tell your body to make less cholesterol. So now you’re artificially lowering your cholesterol even further. So they added in some car they just drank milk and had some um coconut oil and um and that was it. So it was still you know nearly full carnivore but you know a bit of coconut oil right and and sure enough their their cholesterol level came down into the so-called normal range. You know um their policy was happy and then they just went back to doing doing whatever they want wanted to do which is which is um which is interesting. So, but that’s gaming a system. I don’t think that that’s the right thing to do. I don’t think that’s what people should do. Certainly, not long term, because I actually believe that cholesterol is good for you and your body’s doing this on purpose. And if you just don’t eat for 5 days, that’s what your body’s going to do. It’s going to raise your HDL and LDL and lower your triglycerides. And so, I think that just gaming things just for an effect of a number may actually be detrimental. But, what are your thoughts on that? Yeah. Well, have you got three hours? Yeah, I think this this all started actually for me well firstly doing the bloods as I say and that was like 15 years ago where I realized that the numbers didn’t seem to work when you certainly when the doctor was remote it didn’t match up but it got very stark about six years ago like like I say when I did the diabetes meeting for Sean there was a lot of members who were really into the numbers into the data and they started to to question a few things and the HBA1C hemoglobin A1C uh reading which is okay for people on the standard western diet if you’re vegetarian. For many people it’s okay. Um it’s not reliable though. It’s not a very reliable number. But the point being that I had a lot of people coming on board and they’d say my CGM which I’m wearing all the time tells me on my average is let’s just say for the numbers sake it’s 100. Let’s just say 100. Um and then when I do my capillary testing that sort of backs it up. But Stephen I’ve just had my HBA1C and it’s 120 you know. So, it doesn’t make any sense. Well, firstly, I’m a real common sense guy. So are you. Yeah. I mean, if if someone looks pretty healthy, they probably are, you know, and if you do few tests on them and uh those numbers look okay. Yeah. But I’m still going to go with the clinical presentation. Anyway, that happened more than once. This was this was so common. People saying, I don’t get this, you know, and then I’ve gone and had a full set of labs and I’ve had my fasted insulin, fasted glucose measured. I’m doing really well. don’t think this that’s the best management of my blood glucose ever and my HBA A1C is creeping up so what’s happening well then I went back to my training and I can remember being told about artificially low HBA1C and if someone has a low HBA1C but you’re looking at them and they’re saying oh I’m really thirsty and I’m urinating a lot and I can’t quench my thirst and pretty much they look diabetic you know puffy face and you know bloated stomach is one of those things sadly um you’ve got to look at that HBO and see and scratch your head and say maybe something else is going on. Maybe the red blood cells are are dying too soon. And that’s basically what hemolytic anemia is where your red blood cells don’t last because it’s a calculation. It’s not a direct measurement. Uh a HBA1C it looks at the glycation doesn’t definitely do that but then it factors in a number. So they assume your red blood cells live 120 days. So again, the reason I’m using the same number is just to make life easy for people. If let’s say your score was 120 for your glycation rate, then you said, “Yeah, well, we got to factor that by 120 days.” So it’s it’s one unit per day, but your red blood cells live 60 days in reality, right? You’re going to get a completely different number. your glycation is going to look, you know, a lot worse or a lot better depending if they’re living longer or shorter. And we know this is true because you do what’s called a reticular sight count. And it’s I mean, I think you you get involved in bone cancer sometimes, I think. I’m not sure. And you know the way you diagnose bone cancer is you look at the reticular site and the red blood cell count you know and if it’s um you know if the reticular site number is is going through the roof your body is trying to produce red blood cells in huge amounts but if you got a low red blood cell count um they’re being killed you know this it’s not happening something’s wrong. So you’re either very anemic or even to the point where you possibly got cancer of the bone marrow. So it’s a big deal and it’s not even medically controversial. So what would happen if your red blood cells live longer? Well, you’re going to get an artificially high HBA1C. And lo and behold, that’s what happens. So we do in the bloods and I now try to get a reticular site countdown done. So going back to your gaming the number uh I can say to people right if you want it to be lower um then you’ve got to go back to eating carbs. But you’re not actually curing the problem. what you’re doing is you’re making red blood cells not live as long and uh you can do that which ridiculous thing. Luckily there are labs now looking at what’s called a HBA1C adjusted HBO1C. So this isn’t me just making this theory up. This is in clinical practice. This is what bio medical researchers are looking at where they factor in the life of the red blood cell because there are so many people with these devices in their hands on their arms, you know, thinking of bricking and all that and even Apple watches or whatever who are saying this makes no sense. This number does not match what my ad average daily blood glucose is. You know, the the common sense of it is if you look at your blood every single day for 120 days and then you work out your average and it doesn’t match the lab value, the lab value is wrong. Okay? So, so now we get people saying that, you know, the HBA1C is gone. We’ve got to do something. It must be because there’s there’s not enough instinct. There’s too much blood glucose floating around. No, it’s it’s a number that you’re misinterpreting. I mean, sorry to do there. I’ll you smack your head, but have a look at what’s going on. So, um, you know, I’m I’m finding that very frustrating. If you just take a broad step back, a lot of the numbers are wrong because these reference ranges aren’t optimal ranges in the first place. They’re just averages. And as the population gets sicker, they shift these averages. They, you know, so it’s not, it’s not set in stone. It’s not based on athletic performance. It’s not what a perfect human should be. is what an average person could be. And if you go to a shopping mall, I don’t want to be the average person because I don’t think they’re particularly healthy. And then you’ve got to understand the physiology. So the bane of my life is things like, you know, people saying you’re tanking your T3, which maybe we can come back to. That’s not true on this way of eating. It’s just appropriate and lower. Or you’re worried about your insulin being, you know, too low. Well, that that’s not the case. It’s appropriate. I mean, look at you. You got muscle. I’ve got muscle. you know, many of my carnivore colleagues, you know, looking pretty healthy. If you didn’t have enough insulin, you wouldn’t have enough muscle, just you would waste away. Simple as that. So, we know it’s an appropriate level. And where are they getting this low number from? Well, they’re getting it from the reference ranges. You know, if the range is 2 to 20, well, that’s based Well, that’s based on somebody eating 45 to 65% carbohydrates. Yeah, that’s a great range for those people. It’s not for people eating zero% carbohydrate or 5% because you need less insulin. To me, it’s it’s it’s not even rocket science. It’s just common sense that if you look at these numbers and you think, well, we got to gain those numbers, which is what people are trying to do. Um, you’re looking at it completely wrong. And of course, we know about glucose. If you add carbs, it isn’t even inoffensive. It’s it’s bad thing to do. Just going back to red blood cell production, use that as an example. Um there’s a nine step process to make heem for instance and there’s a an enzyme called L A at the first stage. And what limits that glucose? If you have higher glucose uh in your levels in your blood, then your your red blood cell production, which includes incorporated hemoglobin, obviously that’s going to be kicked into touch a little bit. And we can see that with the MCV, what’s called the mean capuscular value, which is how big your red blood cells are. So when you’re eating carbs, that tends to go down because the hem production is reduced. It’s it’s still viable, but it’s um it’s not optimal. So when you see those numbers going up, I get people going, “Oh, my MCB’s gone up. My doctor says that’s bad. I’ve got big red blood cells.” No, that’s carrying a lot more he because it’s able to do that. And also you’re not you’re not restricting he production at the early stage because your glucose levels are actually appropriate rather than you know inappropriate. When someone says just ah just have a few more carbs what you’re actually saying to that person is let’s increase some glycation. Let’s make all your proteins deranged. It has a such a knock-on effect. It’s incredible. Yeah it will raise your insulin because your insulin is saying this is toxic guy. you need to get rid of some of this glucose, but you’re not actually making anyone healthier by doing that. So, if you look at the red blood cell, use that as an example because that’s what we’re using as a proxy marker. U because don’t forget, when you glycate proteins, you’re not just doing it to the hemoglobin, you’re doing it to things like albamin, you’re doing it to a thing that is transporting so many nutrients around your body. It’s absolutely critical. you’re glycating um you know collagen you so so that’s why people look older when they have a lot of carbohydrates because you you’re deranging all the proteins there all these cross-linking going on and you look older so there’s loads of things but if you sorry I’ve gone off the subject but if you just focus on the red red blood cell you know you’re making 2.5 million every single second red blood cells you’re recycling 2.5 million every single second in that red blood cell there’s 280 million proteins that are called hemoglobin just in one red blood cell. So you’re going to glycate some of that. So once that has happened and because once you glycate which is which isn’t being sticky it’s a chemical you it’s a bond an atomic level. It’s an irreversible bond as well. Uh once it’s done it’s done. So it’s in there. It’s deranging that protein making that protein not viable. And you’re doing that to your hemoglobin. you’re also doing it to the structure of a red blood cell. And we know glycation isn’t a problem for the red blood cell as much as deformability. So when you start to make these cross links, um your red blood cells go into the spleen, go into the sinosoid, and they can’t deform. Now, normally when you say there’s a deformity, you think, well, that’s bad. But not with red blood cells. It needs to be able to squeeze into spaces, move around, be very, very flexible. Once you start glycating can’t do that but more importantly the membrane which has membrane proteins and lipids it starts to lose its deformity which is where you’re gaming the number. Mhm. Because basically you’re saying here’s the red blood cell. We’re going to glycate it with a little bit more glucose and we’re also going to uh called a bit a bit of lipid peroxidation and we’re also going to make that not pass the test. You know, simply put, in the in the spleen, in the sinosoid, there’s a a Disney type sort of entrance fee. If you’re if you’re over this size, you can’t ride. All right? So, that’s what happens. And it gets kicked out. So, it’s not viable. Well, when you keep the glycation and um low, you can see that your red blood cells will last longer, but the level of daily glycation is less. But because we go back to that stupid calculation where we’re assuming it lives for 120 days, it artificially raises the number because you know you’ve got glycation from 150 days but they’re assuming it it was over 120 so it’s a higher number. It’s really that simple. Yeah. So, we’ve we’ve got to get into that and you it it’s just crazy because it’s it’s affecting all the other proteins which is which is remarkable. So, you’re causing all this damage to gain a number. You’re not actually improving the body’s system one bit. Mhm. I saw you taking notes. Sorry, I I’ll take a break. No, no, you’re fine. No, I was I was just going to say too, I mean, you know, the the you know, plant steriles, I mean, people point this out that, you know, the plant steriles are close enough to our uh cholesterol that they can get used, especially in like membranes. And uh so they go into the membranes of of red blood cells, but they are they’re not as functional as our cholesterol. So, they make much more stiff and rigid cell membranes. So, they’re not as flexible and foldable and malleable, and so they they get taken up by the spleen um more readily. And so it’s all it’s it’s you know been shown previously that that people that eat a lot of you know vegetables, seed oils, things like that um plant fats just generally it doesn’t have to be seed oils be avocado whatever that they um that they have an abundance of these plant steriles in their body and they can actually um have a shorter lifespan to their red blood cells. So it’s sort of so the opposite and so you take out those plant fats and you’re not glycating everything. I mean, it’s there’s no wonder that these things live longer and therefore have more time to expose their hemoglobin to the even lower levels of blood sugar that are that are there and then have an artificially elevated HBO C. I mean, we we need to have reference ranges for ketogenic group and even full carnivore group, but at least ketogenic. I mean, that that’s a major metabolic change. And so we’re going to get major major differences in um in the blood levels uh even even the averages and that’s not even to say optimal averages where we even have these for just people who eat whatever done studies in Germany where they just they take people in their 20s normal BMI and no diagnosed medical issues which is it’s pretty low bar to to get over right but when you look at those these nominally healthy people that just don’t have anything diagnosed and are of normal BMI I mean I wouldn’t even qualify technically obese, you know, I’m right at BMI, I I balance between 29.5 and 30 BMI. Um, you know, depending on how much I’m in the gym, you know, but that’s um, you know, but if I’m obese, it’s because I’m more muscular and I’ve been working out more, you know, and so they look at these people just normal BMI, just no diagnosed medical issues, and you get very, very different reference ranges. And so we would get a very different reference ranges if we just took an average sampling of ketogenic or carnivore populations. Well, what if you took that optimal just so you know between 20 and 30 or 20 and 40 and normal BMI? It might even exclude a lot of people that are are muscular, whatever, but just no diagnosed medical issues either. you know, you get you get even different um levels still, you know, and that’s that’s important because doctors are are basing entire treatment protocols on these numbers and these numbers are essentially meaningless in a lot of cases. Well, absolutely. And the thing is I think this adding carbs back in theory, yes, it will gain the number, but it is destructive. It is destructive. And even if you want to get into lipids, you get into the fact that apple, which is attached to LDL molecules, that will be glycated, LP little A, you know, which has um the cringles that there’s still amino acids, they still got nitrogen bases, so they will still be glycated, permanently damaged. Then you get into, you know, the glycated um LDL particles, which people, I think, sort of know is not a good thing. See, you’re actually going to increase all of those things. So, it’s it’s not a simple it’s not a simple equation. It’s not just like one number we’re going to focus on. The other thing is I mean your your blood glucose you’re constantly being told you’ve got to worry about insulin which definitely is a factor but don’t forget you know there are 14 glucose transporters and not one of them is totally insulin dependent. In fact, 13 don’t need insulin at all. And even the major one which people talk about glute 4 has five different mechanisms to transllocate and start to work. And only one of those is insulin. The rest is about movement and calcium balance and uh energy substrate and it’s uh mechanical. You know, if you lift a weight uh you are going to improve your glute for expression. Simple as that. That’s that’s my people on you know uh when I used to do the type two diabetic um system where we’re trying to help them even on high carb before my eyes were opened if they did exercise they did get slightly better there’s a mechanistic reason for that and you know I think this obsession with constantly trying to you know manipulate the HBA1C and also improve your insulin you make your make sure your insulin isn’t low. It’s not suppressed or whatever. Well, that that’s just looking at a tiny part of the whole thing. And your glucose management is is more than that. I mean, the passive diffusion of glucose into cells is not accelerated by insulin. So, if you’ve got a low insulin state, you’re going to have slightly more blood glucose floating around. Also, if you’re eating more fats, as you’ve just said, you know, every cell is going to be full of fats for energy. So, glucose isn’t going to go in. I mean, I’m not a big fan of the term insulin resistance. I think it’s physiological protection of the cell. You don’t want an over plus of energy. So, if it’s got enough energy substrate in it, that’s in the form of fat. Why would it let glucose in? It doesn’t need to do that. It’s protecting itself. So, I don’t think that’s insulin resistance. I think that’s physiological adaptation to a highfat diet make again that just makes total sense to me that you would have a cell looking after itself. So I don’t think raising insulin it’s a bit like you know it’s a it’s another way of looking at something like metformin which is really forcing glucose into cells where it shouldn’t be. I’m not a fan of metformin. You can probably tell and it works on the EMPK um you know the the enzyme there that will basically say um although we have enough energy in the cell, we’re going to force even more glucose in. So yeah, again, you gain the number with metformin. You’ve taken it out of your circulation, but you put it into a cell that doesn’t want it. So I’m not a fan of that at all. I’m not I just want people to realize that we’ve got to start doing some joined up thinking not look at one number or two numbers but actually think of the mechanism behind it. I mean that’s the great thing about the hematology side of um you know blabbotomy is you can reverse engineer what people are saying when you look at well why because that’s what I do you know I know I did a decade of private blood testing where it’s no good to say to someone that’s high that’s low so that’s okay because that’s gone up that I I want to be able to explain to people it’s because this has happened that that’s changed not the other way round you have got low triglycerides because you’re not eating carbohydrates. So, your body isn’t changing the carbohydrates or fats or whatever and making more triglycerides that way or whatever whatever the thing is that you want to say to someone in a very simplistic way. But I think that that’s the thing. So, when someone says to me, uh, you know, use T3 maybe as an example, my my T3 is tanked. Right. Well, how are you feeling? Well, I feel great. And this happens honestly this happens in our school communities. so much. Uh, and last night I was asking questions, have you got this, have you got that? You know, unexplained weight gain, weight loss, you know, cold, hot temperature. They were worried about their thyroid and they were just answering in the chats. They didn’t want to do it on the video. No, no, no, no, no. Quite funny really. If we’ videoed it, we went through every symptom of a thyroid problem. They had none. They and at the end they said they feel really great, but the number was bad. Someone had said the T3 is too low. Well, it isn’t too low. I mean, you need a certain amount of T3 when you have a lot of carbohydrates, simply put, because T3 works in glycolysis. It moves the pyuvate across the mitochondrial membrane. You need a lot of T3 to do that. Well, if you’re not relying on glycolysis, you don’t need so much T3. So, using your example there, the reference range is wrong because it’s not appropriate. I’m going to be cheeky here. I mean, that’s why I wrote that book, Guide to Blood Test, in the context of this way of eating is because um there’s so many of these anomalies where the reference range is so irrelevant, but it scares people and you know, the lab will put a big red flag on it. The physician, you must come in and talk about your thyroid and you’ve got no symptoms, but you’ve got a really low, you know, low is the wrong word. You’ve got an appropriate T3, but according to the range, it’s low. Um, and Oh, sorry. Go on. No, you you carry on. Well, no, I was I was just going to say, you know, and and the thing is is that I I do hear that detraction that, you know, you go on a ketogenic diet, it’s going to tank your thyroid. And of course, there, you know, um, you know, as you’ve mentioned, this can be very appropriate. Professor Finny has actually shown this in in several of his papers. um that in a ketogenic state, you simply don’t need as much thyroid hormone to affect the same physiological benefits and metabolic uh stimulation. So, there’s that. But the other side of it is I actually treat a lot of people that have thyroid dysfunction and they have low T3 and they have high TSH and all these other sorts of things. And some of them are outside of the reference range and some of them are just outside of the optimal reference range so that their doctor says your thyroid is fine but they’re symptomatic and they have all these these symptoms, you know, these signs and symptoms that they’re low thyroid. And so I look at that under an optimal sort of reference range for the general public. It’s not even optimal for anybody else, but the but you know when they first come into me they’re they are the general public and and they’re outside of that optimal range. Okay, so we talk about that. But when I put them on especially a carnivore diet, so a plant-free ketogenic diet, I almost always see their thyroid improve and their TS uh um T3 as well as TSH and T4. And there’s a lot of reasons for that. Number one cause of hypothyroidism is Hashimoto thyroiditis, an autoimmune condition that carnivore diet seems to help quite a lot and lower those antibodies down, lowers the damage, and your body can start reversing this damage and start improving function. Um they’re you know getting rid of plants plants. There’s an entire category of plant toxin called grogens. People can just Google that. You know go on chat GPT and say tell me all the different plants with high levels of grogens. They will be all the ones that are in the produce aisle. A lot of leafy greens and things like kale and broccoli and so on. And these block iodine from entering the thyroid and being utilized to make thyroid hormones. You may need an abundance of iodine. Maybe you don’t have that. Um, and um, and then you can maybe have low iodine, but at the end of the day, when I when I get people on there, I almost always see their levels improve dramatically. And and I see sometimes their levels change when when they start adding things back in and their TSH starts climbing up. And um, and people don’t even realize that all the anti-nutrient effect of plants for medications as well as nutrients. I have patients with on thyroid medication. I had a lady the other day TSH in a general range would be between you know 4 and four or five it’s pretty average but optimally it’s it’s between.3 and 1.5 above two can actually double your risk of developing thyroid cancer so that’s clearly not an acceptable range again that’s this normal range but it’s not necessarily an optimal range thyroid cancer is very rare so double a small number is still a small number but it’s still expressing uh the fact that there’s some physiological stress that’s being uh put on your undue stress putting on your thyroid and her TSH and she was on actually quite a high dose of thyroid medication. She’d been on for years. Um and she’s hasn’t really been able to stick with a carnivore diet. We’re sort of, you know, working on that. And um her TSH on this medication, same same dose she’s had for years, was 56. Right. Wow. Wow. any any range you look at that’s the best that’s that’s that’s bad. Yes. Right. That means that you know the body’s really really really trying to work expressly hard to to get something done. Anything done and her T4 and T3 were actually actually quite low and she was quite symptomatic. Turns out she was having coffee with her thyroid medication. coffee is is replete with these anti-nutrients and um and so I’ve found in my thyroid patients that you have to delay about two hours um just through trial and error we found that out that that was that was sort of the sweet spot that wait 2 hours after you’ve had your thyroid medication before you have coffee and you know half an hour before you have anything besides the water and I talked to her and I was I said hey you know were you able to able to to do that and delay she’s like ah well yeah sometimes you know, sometimes an hour, sometimes two. You know, it’s like it was like she wasn’t even as rigid about it. Just changing that, just the timing of her coffee, she her TSH went from 56 down to six. So, and her T4 and T3 both came up. And so, still not not where I wanted it to be, but massive massive difference um and improvement in that as well. But um but yeah, I just wanted to sort of mention that that I actually see a lot of people improving. I mean, my my um you know, every time I tested my thyroid over the last sort of seven years, I think maybe three or four times I’ve tested it, it’s always been in that optimal range uh for, you know, the the general population. These studies have done out of Germany looking at sort of the optimal 25year-old hormonal pattern with normal BMI and and uh no diagnosed medical issues. That’s um mine’s been consistently that I I don’t see too often people actually have low levels of T3. I I know I’ve heard of it, but I haven’t really seen it too often. And and then I’ve seen other times um you know people massively improving their testosterone, double even tripling their testosterone sometimes. And then you’ll get a one-off every now and then. They said, “Oh, my my testosterone didn’t really do anything, but I feel so much better. I’m I’m losing weight and I’m putting on muscle and I’m it’s really easy that I’m able to go harder at the gym and it’s easy for me to put on muscle. It’s like well then who cares? I mean that’s that’s what you want. I mean we’re not going for the high testosterone award you know as far as I know that’s not a thing. You’re you’re trying to you’re trying to be healthy and you’re trying to as an athlete perform in your sport. But at the same time the majority of people I see do increase their testosterone dramatically and get the physiological benefits. And then sometimes you get the physiological benefits, but you don’t see that massive doubling or tripling in your numbers. And you know, famously Sean Baker tested his numbers the day after he did a heavy workout, which actually can lower your your levels. So, um, if he tested again, who knows? But I mean, the guy’s yolked, you know? He’s an absolute moose. And like, I’ve worked out with him. That guy is a beast. He is really strong and he has a lot of endurance and strength endurance. the guy just keeps going and um you know the idea that that that dude is like physiologically low testosterone like is is just a joke. I mean like whatever that guy has that’s exactly what he needs because he’s killing it. And you know something he pointed out was that your testosterone receptors increase when you have more dietary carnitine and carnitine is very very um abundant in red meat. And so he’s obviously going to have a lot more testosterone receptors and you can have the same level of testosterone, double the receptors, you’re going to get a near doubling of effect as well. Absolutely. I mean what is in the blood is not what’s in the tissue. That that’s true of all the readings. I mean just quickly I want to go back to T3 for for one second because there is uh one of the other things people talk about is that gluconneioenesis is stressful which is personally ridiculous in in its entirety because we do it when we’re asleep everybody does it whatever way they’re eating gluconneogenesis is just a physiological process they were particularly worried because firstly oh I’ve been told I’m stressing my body out because of gluconneogenesis and my T3 is low so I’ve got to increase my T3 and I just pointed out you do realize that one of the things T3 does is it stimulates gluconneioenesis which is you know the ridiculous thing and u this was actually an influencer who booked me privately and uh I said yeah I’ve seen some of your stuff and you need to stop saying that because T3 two of the primary things it does is glyco u glyco geolysis you know it will take your glycogen strip it down and make glucose and it will do gluconneogenesis. Well, I didn’t know that. I said, “Well, you shouldn’t be talking about T3 the way you do if you don’t know what it does.” So, what you’re actually saying, you know, when I’m watching you is, you know, you need to not be doing gluconioenesis because it’s stressful. So, therefore, have some carbs and also that will put your T3 up and then you’re actually making your body produce more glucose by gluconogenesis as well. So I think the joined up thinking what you just said about you know the infamous pencil neck Sean Baker you know and his low testosterone it you only got to look at the guy like you just say and say you know the testosterone values don’t really matter because it’s worked for him but you added the mechanism as well. So for the people that want the common sense with the mechanism, the mechanism is always there to explain all these things. If something’s electrically low or high, um, you know, problematic, oh, this is a compound we shouldn’t be making in our body, whatever. The body’s really smart and you’ve got to look at the outcomes. You know, the old thing when computers came in, there was a thing, wasn’t there, where it was a garbage in, garbage out. If these computers aren’t great, you know, they’re not magic. If you put the wrong information in, you will get the wrong information out. Well, the body’s the same, right? So, you can’t look at Sean and say he’s doing the wrong thing. You You just can’t. So, but I can certainly go into a shopping mall and go, I think that person over there is probably doing the wrong thing, and I think that one there is right. I I know it’s bad to judge a book by its cover, but that’s the best thing we got, isn’t it? So, um that’s a common sense start. And then when you add the mechanism, you you’re golden, I think. Well, and we we do spot diagnoses all the time in medicine. I mean, there’s this thing is like, okay, here’s a picture. What’s the diagnosis? I mean, that is actually how we are trained and there are certain things that you can see from someone’s appearance and you can actually get quite a lot of information and we are taught during the physical exam when you walk in the room, you you see what’s going on there. Are there any anything around the bed? Is there like a bunch of snacks and cupcakes, a pack of cigarettes? Is there, you know, a bag of uh, you know, IVs hanging there? You know, is there, you know, what does the patient look like? You know, all these different sorts of things. You can actually gain a lot of information there. And, um, and so, yeah, just looking at Sean Baker and just being like, that guy’s yolked and absolutely killing it. Uh, for any athlete, but certainly, you know, at his age that obviously there’s no there’s no issues there. like he’s he’s very healthy and he’s a lot healthier than he was. And that’s the important thing. That’s what he talks about that even when he was still competing at a high level athletically, he was he was well overweight. He had a lot of excess body fat. He did not feel good. He felt, you know, very unwell and and now he doesn’t. So, you know, that’s um that’s very important, too. I have seen recently um and I’ll get I’ll get you to comment on this too. I’ll give a bit of thoughts and then um see what you have to say, too. But I’ve seen a couple influencers online saying um that it potentially wouldn’t be a good idea to do like a ketogenic diet specifically for those sorts of reasons that you talk about. Well, maybe it can elevate if you already have high cortisol. Well, maybe it can elevate your cortisol more and so this might not be a good idea or you’re already suffering with hypothyroidism so this can also suppress your thyroid even more. We have so there’s so much complexity especially to hormones and different physiological systems in our body. I mean, we’re talking about a system with tens of trillions of cells and trillions of interactions, chemical interactions, which in within each of those cells every second. There’s no chance that you’re going to look at one mechanism and go like this explains everything. You have to know all the knock-on effects, and no one will ever know all the knock-on effects. You learn as much as you can and learn how these things fit together, but there’s there’s always a question of and and then what? And then what? Okay. Oh, so if you do X and you know if you do X then you’ll get this result. Okay. And then what? And then what happens after that and after that and after that and after that and you’re like come around full circle like well actually we don’t want to do uh some whatever X. Um, you know, I’ I’ve I mean, there are plenty of studies, you know, uh, Richard and I, Richard Smith and I did a whole like two and a half hour podcast on this whole idea, you know, the whole Ray Pete idea that, um, you know, ketogen keto poisoning or whatever the hell, you be in ketosis for too long and this causes phys physiological harm. And that’s something that that a lot of people have have bought into. We we went through two and a half hours going through all these arguments and showing direct evidence in the literature of of better studies, higher quality studies with more people over a longer period of time uh in experimental data sets showing the exact opposite of what these claims are making. like a two-year study following people on ketogenic diets that um did not elevate their cortisol, certainly not to cushoid sort of levels. Um but they were just normal and their thyroid did not actually decrease. It actually stayed optimal and a lot of other things improve. Um and so and like you said, you know, um there could be reasons why these things are changing. One reason for cortisol going up in some populations is that when you have metabolic syndromes, you’re metabolically sick, maybe pre-diabetic or diabetic, cortisol actually gets suppressed and you need cortisol. You know, you need the appropriate amounts of cortisol. And then correcting that metabolic syndrome and pre-diabetes can actually normalize your cortisol. Oh, you see it go up. Up is bad. No, up to a great degree in a great extent is bad. But if it’s just renormalizing, well then that’s normal. And then um the other thing is is that we actually use in western medicine right now ketogenic diets to treat Cushings which is very high cortisol levels. You know tumor that makes your body secrete excessive amounts of of cortisol or or Cushingoid syndromes where you have excessive high cortisol for other reasons. But it is in the literature that you can treat people with ketogenic diets um giving them ketogenic diets for Cushings um or hypercortisolia uh because it actually ke being in ketosis actually amilarates the effects the negative effects of high cortisol in the body. So this is something that we actually put people on straight away and then do some definitive treatment like pituitary surgery or something like that. This is actually Cushings. Um and then of course T3 being low. Well, why would you why would you not go on keto just because your T3 is low or or your hypothyroid? It could be something that you’re doing um you know like maybe you have Hashimoto’s or maybe you are eating a bunch of grogens and that’s what’s actually causing you to be hypothyroid and and going keto or carnivore is exactly what you want to do to improve your thyroid function. Um but you know, what are your what are your thoughts on on that idea that you shouldn’t do keto? um if you’re sort of in those categories or or other categories or are there are there categories that you would consider this hey this keto carnivore is not for you. Hey guys, just want to take a second to thank our sponsor at Carnivore Bar. I don’t promote many products because honestly all you need to be healthy is to just eat meat. For those times that you’re out hiking, road tripping, or stuck at work and you want nutritious snack that is just meat, fat, and salt if you want it, the Carnivore Bar is a great option. So, I like this product not because it’s just pure meat, but also because I want the carnivore market to thrive as well. And the more we support meat only products, the more meat only products there will be available in the mainstream. So, if this sounds like something you’d like to get behind, check it out using my discount code Anthony to get 10% off, which also applies to subscriptions, giving you 25% off total. All right, thanks guys. Well, uh, I was taking notes, Anthony, because there’s ever such a lot there to unpack. I mean firstly cortisol is essential for protein metabolism. All right. So we need it and I think these these people are very much uh unable to listen to themselves because they’re also the people that complain about uh adrenal insufficiency as well. So there’s not enough cortisol or there’s too much cortisol. Of course, the problem is chronically elevated levels of cortisol which and what do we call chronically elevated because we go back to those reference ranges. And I I’ll use this as a simple thing to say because if you go to the dentist, if you look closely, you will see a glucagum injection, okay, to raise blood glucose, not cortisol. And there’s a really good reason for that. And the reason is cortisol isn’t the main driver of glucose production. Glucagon is I think everybody knows that. All right. So, so firstly they’re looking in the wrong place. Secondly, there’s medically proven mechanisms. Like I say, the dentist is the easiest one because they make it really available because they need it, right? So, you would think that um you want to raise blood glucose quickly. It would be cortisol. So, there’s a common sense thing. Secondly, like I say, it’s involved in protein metabolism. We eat more protein, so we’re going to need more cortisol. All right, that that that’s another thing. Um, and T3, T3 will push glucose production up as well. So, what do you want? Do you want to stop the cortisol because it’s making gluconioenesis happen but in the same time add a different hormone that promotes gluconogenesis by raising it’s not it’s not joined up thinking that that that’s the main thing. Yeah. And I will prove where cortisol the production of glucose from cortisol is different. Cortisol has a great effect that nobody really talks about. Okay. So they do talk about fight flight or freeze. If tiger runs in here I know it’s cool need. I’m gonna want to raise my blood glucose. Right. I wouldn’t do it with anything other than cortisol because cortisol is going to stop anything lowering my blood glucose. And you get what’s called physiological insulin resistance. The body’s really smart because if you think about it, the tiger comes in. I need my blood glucose go up. Yeah, I’m going to produce some cortisol, but at the same time, my body’s going to lower my blood glucose. That that doesn’t make physiological sense. So that’s where the chronically elevated issue is and we’re not doing that. We’re not in fight or flight because what’s happening is our blood glucose isn’t staying elevated. We all have very low blood glucose. So it’s not the same mechanism if you get my drift. Because otherwise if if if it was cortisol driven, it would always be elevated because the point of a cortisol uh reacted glucose level is to stay elevated so you can run away and get up a tree or fight. And this is where the anxiety thing comes in in as well. It’s if it’s chronically elevated. If you’re in a job, you you hate your life and stuff like that. Anxiety is is problematic. I’m not saying that that isn’t. But when you’re looking at a cortisol reaction is absolutely essential because the tiger coming in, you need anxiety to make a decision. We don’t have anxiety for no reason. It’s a physiological thing that we need. Without anxiety, I just go, “Well, there’s a tiger. Think I might need to do something.” You know, my anxiety kicks in like, “Right, decision time. I’ve got to go.” And this is where if we go back to common sense, this is why people in say a job where their manager they absolutely hate, why their their health is destroyed because they can’t run away. They can’t punch the manager in the face. They can’t say what they really think. So they have that chronically elevated fight, flight, freeze response and a chronically elevated level of anxiety. That’s nothing to do with diet. That’s situational. That’s environmental. If you want to get into the bioysics or you know the biochemistry of it, two different things slightly. Um it doesn’t make any sense that the body would produce cortisol when we need some slightly more blood glucose just to get through a workout you know. So when when you go like I say when you work out as soon as you contract a muscle what’s actually happening more than anything is the glute for expression improves. So the glucose that you do have is uptaken. So you can feel stronger and then then you will get the response from the cellular level and this is where the sodium potassium pumps come in and where the T3 mechanism comes in. So what’s happening at the cellular level is your sodium potassium pumps go you know like gang busters as they say and that’s detected. That’s a that’s a T3 reaction. That’s T3 that’s doing that. Mhm. then and it will it will sense wow the met metabolic rate isn’t where it should be the feedback will say we need more so what will happen is T3 will production will go up it will enter the cell and do exactly the same thing you know go through the transcription factors make the the membrane proteins and produce more sodium potassium pumps and that just gets the whole system going that’s not cortisol driven at all and it’s just it it’s just crazy that’s why you come out of the gym I’m feeling good. You No one ever says to me, I tell you, when I was an advanced person, advanced personal trainer, I had many people say they don’t fancy working out today until they’d worked out. And I never ever in all those years had one person ever say to me, I really regret doing that ever. So, um, how So, if it is cortisol, firstly, that’s proves it it’s not all bad, but secondly, it isn’t cortisol anyway. You get all these good effects. You get indogenous morphine, which people call endorphins, you know. So, this is this is what frustrates me so much. You can probably tell from my body language that it’s not understanding what’s going on. It’s making this, oh, cortisol is a stress hormone and, you know, it’s really bad and it’s produ producing lots of glucose. No, it’s not. It is in certain situations. Uh, that’s when it’s and when it’s needed. You know, if you can react when it’s needed, that’s good. But when you’ve got the environmental stress is is the key here. So if you’re in a job that’s really bad, I tell you what, any way of eating is not going to make much difference. I think carnival will make you more levelheaded. I think you’ll be less inflamed and maybe you’ll be able to cope with it a bit better, but in the end, you know, in life, you must get this answer. There are certain things where diet isn’t the thing. You know, we were talking about personal grief. You know, if you got some grief in your life, having a ribeye might be marginally better than having, you know, fruit salad, but you still got the grief. So, you’ve got to deal with the actual thing that’s causing the stress in the first place or, you know, the way you think about it. But, but looking at it as a sort of um, like I say, biochemistry thing, cortisol is not the enemy. And we need cortisol. Cortisol is there for a reason. It wakes us all up. I mean, you know, it has that effect. Again, there’s there’s a great example. If cortisol was bad, you know, um it would it would raise your blood glucose, but then it it’s got to it’s got to do its job. It’s got to keep it elevated. So, it makes you and I hate the phrase, but let’s use it. It makes you insulin resistance temporarily. Mhm. Because otherwise, it wouldn’t do its job. Mhm. So cortisol is there to put your blood glucose up to wake you up. So we have it every single day. Now when we do the a dional testing and we see that beautiful shape, you know, like a sort of ski ramp, that’s fine. You don’t go, “Oh, look at it’s really bad in the morning.” We all say, “Oh, we know what that is. That’s to get you up.” So cortisol isn’t the enemy, but if we didn’t see that beautiful shape, if we saw it across the day, it wouldn’t be being in ketosis. that’s caused that. Absolutely not. It’s not the stress of gluconneogenesis that’s causing that. Absolutely not. There’s something else going on in your life. Absolutely. Yeah. Well, and also that’s you know the um the confusion there as well is first of all a being in ketosis does not elevate your cortisol past physiological levels. A Mhm. B it can ameliate super physiological levels of c cortisol and c stress can increase cortisol levels but increased cortisol levels for other reasons does not cause stress and that’s a problem that people people look at cortisol and stress as synonymous and they’re saying that well if you have elevated cortisol that’s mean putting more stress on your system system and if you go into ketosis that elevates cortisol and that’s putting stress on your system. No, like even if this were a physiological uh mechanism to say, oh, we wanted to raise your your blood sugar. It’s not that, oh, we’re going to cause stress and then cause cortisol to go up. That’s actually adrenaline. Adrenaline is is secreted when when uh you are stressed or in that fight orflight sort of mode. And then cortisol actually amilarates the effects of of of adrenaline. So, um I’ I’ve heard people argue that it’s actually adrenaline that’s actually a very serious issue with stress and then cortisol is actually the saving grace is coming in putting out the fire caused by adrenaline as well. But either way you look at it, if if cortisol is going up for a physiological reason, it’s not causing stress. When you wake up in the morning, your cortisol level is up. It’s not because you’re stressed. It’s not because there’s stress there and it’s not causing stress. That’s a normal physiological response and that’s something that people uh sort of get backwards um all the time. Yeah, that’s what I was trying to say, but I think you were more eloquent than me. No. Um I was going to say too, you you mentioned insulin insulin suppression. So, this is something that that’s gone around. I haven’t had heard people talk about this before and I’ve certainly had, you know, my my views on this and certainly never seen anything like this in practice and and um and so on, but I mean the a lot of times people bandandy around these terms and there’s actually no real working definition. It’s say, “Oh, you should eat plants because of hormmesis.” The hell do you mean by hormesis? And then and there there’s tens of thousands of chemicals or hundreds of thousands, nearly a million. What what which ones are hormetic and at what levels and are they? and there’s a thousand in each vegetable and so which one are you which ones are you talking about which ones are hormatic and which ones aren’t and at what dose and how many leaves and like what the hell are you talking about? Sort of a meaningless sort of term. Um and so insulin suppression, you know, is there is there a working definition of this and then what do they mean by that? And um and and you know what would that really mean? Because to me that would mean that if you were, you know, and then if you could go ketogenic or something like that, this could suppress your insulin and you’re not getting enough carbohydrates to boost this. Even though that wouldn’t really make sense evolutionarily because, you know, there were periods of time, vast periods of time, where people were in the Arctic Circle during the ice ages and didn’t have access to any car carbohydrates. And, you know, I’ve looked into the whole glycogen in muscles idea. There’s not much. There’s really not that much. and and um and it goes away very quickly after the animal dies. It breaks down and um and so you’re not you’re not getting all that much in there. And um and so we wouldn’t have had that sort of bonus from carbohydrates in all these these different regions. So if insulin resistance or suppression was a thing, then that would be something that we should have seen and probably bred out and those those guys would have died out, the ones that were susceptible to that. uh but also you know you should see an actual suppression meaning that when you eat protein you shouldn’t actually get a physiological response with via insulin and so you can do sort of a a modified you know toler you know a glucose tolerance test or protein tolerance test or a craft test where you have protein and you see you know is your insulin rising to to physiological amounts I mean that’s sort of how you would have to prove that I think um but what are your thoughts on that and is there is an actual working definition or is this sort of just like a boogeyman like hormesis? Yeah. Well, it’s a theory where someone’s looked at a reference range and thought it’s really low and said, “Oh, it must be suppressed.” It’s it’s it’s a firstly a ridiculous um assertion because you’re not looking at the reference ranges. And I think it’s been linked to like I say the unreliable HBA1C where the HBA1C’s gone up or or maybe the blood glucose circulating’s gone up slightly. It’s not really understanding as I say that you know the we have 14 glute transporters of which only one is insulin dependent and it’s not totally insulin independent either. So I don’t think I don’t think it’s understanding how we get glucose into the cells. Um so when they see the low level I mean we use yourself or Sean as an example or myself. If I was insulin suppressed I would not have I wouldn’t have muscle mass. I mean it’s it’s really that simple. That’s one of the things that um insulin does. So it it well really actually it’s an anti catabolic effect of insulin. We know it’s anabolic. But let’s look at it the other way. If you have, you know, uh low levels of insulin, your body would be eating itself. If it was inappropriate, if it was suppressed, you would you would have muscle breakdown because insulin prevents muscle breakdown. So I’ve got very low insulin. I’m not losing muscle. In fact, I’m gaining it. So, I can’t have a suppressed level of insulin even though it’s allegedly low. You can’t insulin because look at you. You’re pretty jacked at the moment. I don’t think you’ve gone to the gym much. All right. So, so insulin’s protecting you from losing the muscle that you got. Sean Baker be another one. So, um, if we look at the function of insulin, then we can decide is it suppressed? Is it low? Is it problematic? Well, that’s a big one for me. Like I say, you look at, you know, Richard Smith, very low insulin. Then you look at uh say electrolyte balance. It regulates sodium for instance. So we all know carb face you know most people seen the memes or carb face low carb face and it’s you know there’s no water retention. It’s not all puffy. I don’t think I’ve got a puffy face. Don’t think you’ve got a puffy face. So I think our sodium balance is good. Our electrolyte balance is good. So we’ve got appropriate levels of insulin. And I’m going back to this theory is being postulated by people that don’t have this symptomology. They don’t have muscle breakdown. They don’t have puffy faces. You know, they that it it you can tell I’m really struggling to actually see any validity in it whatsoever because they’re looking at numbers and that’s not the story. It’s an anabolic hormone. if you’ve got your muscle mass, if you’ve got your water retention, your electrolyte balance right, if you’re still able to build some muscle actually, and I think, you know, Sean’s looking more and more wicked as we go along. Um, you know, so, so I think there there’s too many things that insulin does that we’re doing okay for low levels of insulin to be a problem or for it to be suppressed. I don’t know what the mechanism is. um certainly don’t understand why eating carbs again would be the thing to do. The only reason that would be is to push that um insulin response up and gaming again. It’s just gaming numbers. So yeah, there’s there is nothing to it. I think um I I can’t see any reason um why why we’re worried about it to be honest. Yeah. Well, I mean and and that’s the thing too. I mean you rais you rais a very valid point about the muscle wasting and that and that and true insulin suppression I mean it’s an extreme form is type 1 diabetes is not type 1 diabetes exactly yeah yeah you’ve suppressed your beta beta cells in your pancreas from making appropriate amounts of insulin and you you cannot store uh body fat or muscle and and you waste away and you get very very skinny and um well and you die eventually you do die eventually yeah and and fun fact the only treatment we had for insulin suppression and was um ketogenic diets. I have since the late 1700s to until 1921 when they when they synthesized or or isolated insulin. Um but I have I have Sir William Osler’s medical textbook from 1910 or the edition was the 1910 edition. Um he was the first professor of medicine at John’s Hopkins and he was kned for his efforts uh in medical education. very brilliant man and well and just medical um his medical innovations oser’s nose there’s a lot of things named after him and um he in that chapter he has a chapter on diabetes and the treatment for diabetes the one and only for type one type two they didn’t differentiate was a low to zero carb car d um carb diet with basically equal parts protein and fat and basically you’re doing this from meat it was called an animal-based diet you just ate meat equal portions ‘s fat and protein, cut out the carbs. That was the only thing that kept people alive uh with true insulin suppression. And so these are people who actually were type 1 diabetics and were not able to make insulin and yet they were living 9 months to a year uh pretty regularly. He said there’s a high mortality rate but that you know but that you could extend their life you know 9 10 12 months and that not all of them died. You know people actually lived with insulin suppression. you actually potentially even reverse that insulin suppression. I’ve had two patients now um this is actually in the case literature. There are two case reports showing this as well that people have actually reversed um type 1 diabetes by going on to a ketogenic carnivore diet. And what I think is because it affects type um autoimmune issues so at a root cause level I believe that if you haven’t destroyed those beta eyelet cells completely where they’re just not able to make insulin. They’re insulin suppressed but they’re not completely destroyed that you stop that damage and maybe they can they can regrow. Also the antibodies only damage the beta cells. They don’t damage the beta uh stem cells and that’s really important too. So, if you can stimulate those beta stem cells to make more and you stop the damage from killing all those new cells, well, then you can potentially regrow those beta cells. And I’ve had two patients actually follow that and they went ketogenic carnivore straight away after their diagnosis. And this was born type one. They had antibodies present. They had zero insulin, zero ceptide. Um, they were in DKA, they had polyypia, poly polyura, you know, massive weight loss in a short period of time. It was just classic. And they came to me, you know, a week or two after they got out of the hospital, started them on ketogenic carnivore, started following them. Instantly their blood sugar became much more regulated, using much more regular amounts of insulin. Um, and but then after 6 weeks, they their ceptide actually was present. It was below the reference range, but it existed. And they were using less and less insulin. They were less insulin suppressed. And then 6 weeks after that, so 3 months after we started them on the plan, they uh were had high normal cpeptides, which is which is a marker of your natural body’s ability uh to produce insulin called the endogenous insulin production. And so they had high normal cpeptide, dead normal optimal dare say insulin levels and taking no outside insulin. And um so in by in in real terms they had reversed their type one. Now is that going to persist? Who knows? But right now that’s what’s going on. Um one of those people were were not able to stay on the diet because they worked in the mind sites and had to fly away and couldn’t control their meals. Um and so they came off of it instantly. Their um they they their body demanded insulin and their blood sugars were all over the place and they’re having a hard time with it. And after a couple months of this, they said, “No, I have to I have to figure this out.” And they started bringing food in and all the rest. And about 3 months later, again, he was able to normalize his ceptide and endogenous insulin production. And he was off all his insulin. His hbc was 4.5, right? So people saying that no, no, no, he’ll still have to have insulin because um he won’t he won’t be able to get proper glucose control. Sorry. His glucose is better than yours. and um and he’s a continuous glucose monitor. There’s no variation, just dead flat the whole time, you know, very low levels and and constantly. So, so to me, that’s that’s real insulin suppression. And um ketogenic diets and carnivore diets actually treat that. Yeah. And it’s good way of flipping it. I mean just for for people who are not sure what you’re talking about the C peptide the C stands for connected because in the vesicle it’s connected to insulin and as it comes out the vesicle off goes insulin but it has a a a very rapid halflife in the blood so it’s difficult to measure compared to ceptide so it’s a great pro great proxy marker for insulin production and um I mean one of the things by the way but when I was doing my personal training and I used to take this book out which is medical physiology and um well the reason is I used to say, “Look, you can book me for lots of sessions if you want to lose weight, or you can read this chapter on um or even just these highlighted bits about insulin and how low insulin is excellent and uh increased metabolic use of fat is caused by insulin lack. You know, actually says that um so it’s known the effects of insulin or fat storage and synthesis. This book, the entire book is all about um the physiology of the human body. But when it gets into insulin, the only thing it wants you to do is have low levels, appropriate low levels. Um so I think it it’s a theory that doesn’t even pass the the scratch test, you know, as soon as you start looking at it. Like I say, adding carbs back in is problematic. Trying to manipulate the insulin number when it’s inappropriate. You know, I’ve seen influencers say, “Yeah, look at this guy. He looks great, but his insulin’s really low.” Oh, I think, well, of course, look at him. He looks really great. You know, he’s got muscle mass and low body fat. That sounds pretty good to me. I think his insulin is at the the sweet spot. I think personally, I don’t think it’s low just because it doesn’t fit the the reference range. I mean, going back to your thyroid thing, uh I spoke to Amber O’Harn about this and I had a guy that was meticulous with his thyroid numbers. Normally when we took thyroid is females but this was a guy and he had four years and he had his TSH T4 T3 and also you know how he looked and felt was really important and he came to me because he said four years they’ve been telling me I’ve got subclinical TSH and I’m just so fed up with this because I feel great. I’m like right okay for four years they he’s been nagged. So we looked at his numbers and this is what I said to him and I told Amber about this. She thought it was great. She said u yeah good good thought experiment. I said look let’s imagine you’re the first person that’s ever come in with labs. All right you’re the first person that’s ever done that. Okay. And we looked at your TSH which you’re saying is subclinical but I’m looking at these numbers and I’m thinking what does TSH do? It makes your thyroid because it’s not a thyroid hormone. It’s pituitary gone. It tells your thyroid to produce T4 and little bit T3. All right. And also it does have feedback from the body to tell you what’s going on. So this perfect set of data said for year one you have very low level of TSH which is allegedly subclinical but your T4 and T3 and your clinical outcomes are great. Then it’s the same low low number and the T4 and T3 is about the same and you still feel great. Blah blah blah. Four years right? First time I’ve ever seen bloods. I’m going to work out reference ranges. That’s perfect TSH because it’s got everything. It’s got the level. It’s about the same and the outcomes and the clinical outcomes. So, we got the numbers and we’ve got the real life experience. And that said it all to me. It’s not about the numbers because this guy was living proof. Sadly, didn’t want to do an interview. But it it was amazing because it was there in black and white that the body is is smart. We are so so arrogant to think it’s always going wrong and we can tweak it and can biohack it. You know, when we take like co-actors, oh, I’m going to take this amino acid and this amino acid and it’s going to make this in my body. No, your body won’t necessarily do that. It will do what it thinks. I I’m not a great fan of all the co-actors and stuff like that because the body does what it wants to do and what it thinks is best and you can’t force it to make glutathione or you you can’t make it do what it doesn’t want to do. If if you’re short of nutrients, then it makes sense. You know, if you if you’re not eating foods that got B1 in or B9 or B12 or whatever, you’re going to have a problem. I’m not saying that. But I think um if you are eating this way, you are getting those things, you’re getting all the B vitamins, you’re getting enough folate, you’re getting everything that you need, all the essential amino acids, all the essential fatty acids. Let it just do it, you know, and don’t worry about numbers. If your outcome is great, you know, that’s fantastic. Now, if you’re transitioning, say say, you know, you’re new to this way of eating and you’re having trouble with fat malabsorption, you know, oh, I’m not used to the fat. It makes, oh, I can’t I can’t cope with it. Well, there’s two things you can do. One is you can have smaller meals with a bit more frequency, give your body some chance to do it. Or you could go over your body’s physiological limits and have like ox bile. Mhm. I don’t like doing that either because you’re you’re taking something that you’re producing bile which isn’t up to speed yet and you’re saying here’s my little bridge. So I think I’m not anti people trying to get around these things and do workarounds and stuff like that but in the end uh and I’m going to steal this from Benazardi. Vitamin P is really good. That’s patience. You know just let your body work it out. You know you transition slowly I think. Um, and your body will work all all of these things out. It will give you the appropriate level of insulin. It will give you the appropriate level of growth. It will give you the appropriate level of thyroid hormone. And your body is so good at regenerating and healing. It might take a year, might take six months. But I will go into one little provis. So that being said, it also does depend on your personality. You know, if you’re a personality that can’t moderate and you have to abstain, you know, so I’ll have someone, oh, I used to smoke like five packs of cigarettes a day and I just gave up like that. Well, that tells me that person needs you need to stop doing that and you need to start doing this, but then you just tell them there’s going to be a whole host of toilet issues for three or four weeks and you might feel worse before you feel better. But don’t don’t just go by numbers. Don’t don’t think that you know listen to an influencer and oh yeah my insulin is going to be suppressed. No your insulin is going to be adequate for the carbohydrate intake and and you know even the you know indogenous production of glucose which still needs insulin. So so don’t worry about it. Yeah. Yeah. Well and that’s always what I I try to you know tell people try to do something now that you can continue doing 40 years from now that’s going to still work for you now 40 years from now. eat fatty meat till it stops tasting good. Do that as many times a day as your body’s telling you to and live your life. Exercise, get outside, do those sorts of things. And and you can do that when you’re losing weight, trying to put on muscle, trying to just maintain where you are because your body will tell you sort of how much to eat. And if you’re sort of gaming the system and doing things and and adjusting things in such ways to get faster um you know fat loss or something like that then I mean sure you you could probably do that but that’s not necessarily but then what do you do after that? I mean, it’s not something that you can do forever. And so then you have to go back to doing this. And then is there going to be some rebounding effect where you sort of trash your metabolism and then you have you sort of put back on some fat or something like that or it’s just you’re just not as healthy as you would be and you don’t have the practice and and and the habit of of eating this certain way that you can just sort of continue this forever which is I think the best way to do it. And you know, you what you you mentioned before with you know, the subclinical TSH. I mean, if your T4 and T3 are optimal and you’re feeling great, I mean, that’s that’s fantastic. Yeah. Right. Because that’s my point. Yeah. Well, that’s I mean, that’s why I tell people TSH is basically a marker of how hard your body has to work to make the amount of thyroid hormone that you’re producing. And so, if that’s Sorry, Anthony, can I just pick up on that? But you could theoretically, you know, say that’s TSH suppression. That was the point I was making. Yeah, I was. Yeah, exactly. And so, yeah, you could say maybe there’s a pituitary issue and your pituitary is not able to produce appropriate amounts of TSH or or maybe, you know, pan hypopituitarism. You have all these different hormones. But that would only be the case if you were if you were subclinical on T4 and T3, right? But if you have optimal levels, right, then that then your body is body’s just not having to work hard. Same thing with insulin. If you’re not having to work very hard um to get the physiological effects that you need, you only need a certain amount of insulin. Well, then that’s fine. Even if it’s sort of subclinical. And you know, the the other thing is is that insulin suppression, if it were suppressed, what would be the first thing you’d see? High blood sugar, wouldn’t you? Yeah. Yes. Right. And yet we’re not seeing that. Now, now if someone were now, you know, but that’s the reverse engineering bit, isn’t it? That’s the bit they’re looking at the HBA1C and not realizing that’s unreliable. Well, that’s gone up. So, so it must be insulin suppression because that’s gone up. What you just said, well, they’re they’re putting the cart before the horse and using the wrong metric. That’s it’s like saying, look at TSH cuz look at what it’s doing to your cortisol. Like, oh, hang on a minute. you you’ve really gone off pie here. Yeah. Um you these like you just say if you’re insulin suppressed your blood glucose goes up. Well yeah but that’s not happening. But secondly the theory is saying you’re insulin suppressed your HBA1C’s gone up. No your red blood cells are living longer. You’re not factoring in that thing. Yeah. That’s you know sorry I’m frustrated about this whole thing. It’s a ridiculous thing isn’t it? Well the thing is and we have a craft test right. So, I mean, that’s what you’d want to do, right? You give somebody, you know, some some glucose, sugar, whatever, and and then you check their blood sugar and their insulin. And then a couple hours later, you check their blood sugar and their insulin. And then 5 hours, you know, blood sugar and insulin, and you see see what the blood sugar is and what the insulin response is, and is there an appropriate drop in your blood sugar, is appropriate rise in your insulin, is there appropriate drop in your blood sugar, etc. And so if you sure if you saw that after 5 hours your insulin had barely come up and your blood sugar had stayed elevated well I agree you’re not making enough insulin aren’t you right? It’s so simple isn’t it? Yeah. And but but that that is what you would see and you know you you do see that like actual um you know insuffs insulin insufficiency where someone could be a type one or type two diabetic for several years or decades and they sort of they’re running at such high insulin levels for so long that they actually start burning out their their beta eyelet cells. And so you you do some see patients sometimes, I’m sure you’ve seen many of these where they actually do have lower insulin levels, but their blood sugar is very elevated and uh and their HBOC is actually, you know, appropriately elevated. You know, they’re that 9 10 something like that, 11, but their insulin is just not cutting the mustard. But again, the treatment for that is they’re on a ketogenic diet and that sort of reverses that diabetes. And the Harvard study showed that 100% of diabetics um that were on injectable medications like in injectable diabetes medications like insulin, 100% of them came off 100% of their injectable medications, right? Which is which is pretty which is pretty significant as well. I think it is rather it could get any better, could it? And and the other thing with with insulin suppression, just not not to beat a dead horse, but the one thing that that sort of confused me about that is that why is this being suppressed for protein and not carbs, right? I mean, the answer to this was to add in, you know, you know, uh, you know, uh, um, you know, fair enough, low amounts of carbohydrates. And they’re not telling you to, you know, dump in, you know, 200 400 gram of carbs like some people say, but but add in carbs and to stimulate that insulin. Okay. Well, why is it why is it suppressed for protein and not and not carbohydrates? Why is carbohydrate and and how does that reverse the suppression? What is suppressing the insulin? Why is it suppressed for protein and not and not uh carbohydrates? Or is it that you just get such a massive spike from carbohydrates that it’s forcing the suppressed amounts of insulin to get up to, you know, where you want it to be? Um, and then and then how does eating carbohydrates then reverse that suppression? You know what I mean? I mean, there’s no there’s no me. Yes, I know. Exactly what you mean. I know exactly what you mean. It’s a it’s a bit like, you know, what they’re saying is, can we have an appro inappropriately higher level because your insulin is is being released at an appropriate level. That’s what’s happening. Exactly what you just said. There’s no carbohydrates. There’s protein and fats. That’s the amount of insulin we need. Just look at our clinical outcomes. It’s a bit like, you know, when you you go to the gym and you look at some weights and uh it might be some influencers weights that have got a certain number written on, but they’re actually much much lighter, right? If you went to pick it up, you well, you pick it up like you were trying to throw it because your body had prepared for a much heavier weight, you would be inappropriate. So what what you’re doing is you’re doing an inappropriate release of your energy because you’re expecting more, right? So what you’re doing with this insulin suppression theory is saying, well, you only need this amount, but I think it’s low, so let’s artificially have more insulin than we actually need, you know, which is crazy because all you’re doing is you’re saying, right, here’s your your glucose concentration, here’s your muscles, here’s your homeostatic sort of where you are at. you your body fat is where it is. Um, what we’re going to do, we’re going to put some carbs in and that will raise your insulin. Well, actually, it’s it’s complete the net effect is completely negated because you put the carbs in and the insulin raises to work on those carbs and brings it back down. Once you stop eating the carbs, it be back where it was because insulin is responsive to the biochemistry that’s going on and and likely to biohysics. So, it it’s it’s pointless. It’s a pointless exercise. Exactly what you just say because it’s the the pancreas isn’t going to go woohoo. We’re making so much more insulin. Way happening, guys. Let’s keep it up. It’s not going to do that because the body is so smart. It doesn’t waste substrate, doesn’t waste energy. Um, and like you say, you know, true insulin suppression is type 1 diabetes where you can’t make enough. It is a a name that’s been added to something that is just a physiological response. We live in a lower insulin environment. It doesn’t matter about the reference ranges. The HBA1C is is misleading for people. And also, you know, the what should our blood glucose be? Well, people think it should be under 100. Nice arbitrary number, isn’t it? It fits really well. Unless you’re in the UK where it’s minimals and completely different. Um, but who says why can’t it be 110? Why can’t 110 be okay? Well, maybe in a low insulin environment with optimal health, it’s probably all right. It’s probably quite good. I mean I would only worry to be to to be frank and we know this from clinical experimentation that 100 I’m not saying to get to 179 for instance but 180 mgrams per deciliter is roughly where um the excess glucose starts going into your urine which is you know the classic symptoms of of what actually diabet diabetes malatuses is which is a a combination of Greek and Latin which just means passing through honey tasting piss basically sorry to swear but that’s what it means. Um, you know, so maybe we should go back to the fact that that’s how they used to diagnose diabetes. Have you got sugar in your urine and are you you’re not not looking healthy? Um, because the numbers are mis are misleading people. They are definitely misleading people. Don’t worry. And also maybe look at the context. You got 5 lers of blood and I use this to get across what concentration of blood glucose means. So you’ve probably got about 5 lers of blood, right? And then you’ve got a kid next to you who’s 10. They’ve got three lers of blood and you got two cans of Coke. Both have got 19 nine teaspoons of sugar in. Right? So I take it. Wow. Nine teaspoons in five lers. Why is that kid hyperactive? Because it’s three liters with nine teaspoons. So the concentration from this one inoffensive can of Coke is really bad for that child. So maybe the concentration of glucose is is okay at 110 because we’re not talking 9 teaspoons. We’re talking from 100 to 110. We’re talking one teaspoon of sugar in 5 L to one/10enth of a teaspoon in 5 lers extra. It’s it’s not a lot. I I personally wouldn’t worry. And and if the American look spoke in millim moles, you know, it doesn’t sound so different. 5.5 to 5.6 is not much, is it? Mhm. But 100 to 110 sounds worse. But if I think if you did a sort of lab experiment where you put five lers of fluid somewhere and you had a pipette and you dropped in five, you know, five grams and you said, “Oh, wow. Look, you’re worried about this and you squeezed a 10% of the pipet in there.” People would go, “Not it’s not really that much, is it?” So, um, I think it’s just sort of trying to get the frame of reference right. you know, so I I think that that’s one of the things. I mean, I know it’s not the greatest analogy and it may be a bit patronizing, but you know, it’s also over time, isn’t it? So, if you keep if you kept it at 100, say, for 24 hours and the next 24 hours, the next 24 hours, there probably wouldn’t be much difference between that and maybe 110 over hours and hours and hours and days and days and days. I don’t think there would do me much difference. I think the body will probably cope with that. Okay. Especially if you’re fat adapted. Um but it it it’s it’s beyond me why it’s got got any traction because it just doesn’t make any sense to me. Just doesn’t doesn’t do anything for me whatsoever. There are so many myths of with this way of eating, you know, like iron overload and you know, that’s another one that keeps coming up and people don’t get the right panels and they don’t look at the right things. They just read I’ve got red me red meat and there’s loads of iron in that. It’s going to be a problem, isn’t it? Mhm. Why? Yeah. Well, and and like to your point, I mean, I have I have patients with with um genetic hemocromattosis with, you know, phenotypical sort of presentation where they they have um iron overload, actual depositions in their organs. They have to get regular um blood draws. And then I have people that don’t have the genetics, but phenotypically they still get overload and they get um uh they have to get uh every every two months or so they have to get their um uh their blood drawn. And when I put them on on carnivore diets, eating just red meat with all the bio the most bioavailable versions of of um iron, just hem iron, um actually their feritin levels uh come down and normalize and they stop actually depositing. actually reverses this um uh this this iron overload. And and so yeah, there’s there’s a lot of these things. And you know what I what I explain to people is that it’s not about how much iron you’re getting in your diet. It’s about how your body processes that iron, utilize that iron, metabolizes that iron because in hemocromattosis, you’re just not letting go of it and you’re it’s you’re you’re you’re depositing in places it’s not supposed to go. So there’s there’s physiological dysfunction there. It’s not because you’re just eating too much. I mean, if you’re massively supplementing or something like that, you know, I’m sure you can cause problems, but not from from our physiological diet, just from a normal amount in our diet. And um you know, to your you know, it reminded me of something when we were talking about HBA1C was that athletes can can typically make higher blood sugar. They actually in while exercising, it’s very normal for athletes who wear CGMs to see that blood sugar level go up. And if you’re like someone like Dr. Baker, who has said he wears a CGM and he when he’s doing a really hard workout, just going crazy on deadlifts or rowing or whatever, he can actually see that go up to 200 on his his blood sugar. And so, but that’s physiological that that’s what his body is is doing. So, if someone is is working out a lot, um especially if they’re working out every day and they’re getting their their blood sugar levels physiologically coming up, that could also alter the HBA1C. So, it might be that in in passive sedentary populations that are on ketogenic carnivore diets, um, you may not see, you know, any any issues with HBA1C, but, you know, I’ve eaten the exact same thing for basically a decade. And my my my HBA1C will actually still fluctuate to this day. And so, it was like, okay, well, why the hell is that? Okay, well, maybe some stress, maybe some sleep issues or whatever, and um, you know, jacking up cortisol or whatever. But um it could also very well be uh something to do with exercise and uh during periods of time where I’m more active and lifting weights or playing rugby uh could could very well be higher levels of HBA1C. And um you know thinking back on that during those periods when I was lifting weights basically four or five days a week playing rugby 3 4 days a weekend um that was when my HBA1C was was higher than other times. Never high but it was it was higher than other times. And then other times when I hadn’t been able to work out and exercise and been more sedentary, um it had just sort of just come down. Don’t know. But yeah. Well, there there’s Yeah, there’s so much to the variation. It’s if it’s unlikely it’s going to be dietary to be honest. And also red blood cell lifespan is going to affect that and enzyatic um reactions and damage. So for instance when you do physical activity um yes you will get more uh glucose going into the cells and there’ll definitely be more blood pumping around but you also get more damage as well. So you may have actually been at some point where uh your body was um coping and there was less damage. So the red blood cells they secrete a substance phosphoridosine which which is from their membrane which says to the spleen we’re broken you need to eat eat us up. So it could be a day old. I mean, it really could be. Um, and that’s going to mess your figures up. So if it, for instance, you know, if you you had a side injury, someone runs into you in rugby, you’re going to get damage, but you’re going to get damage to red blood cells as well as every other sort of thing. And this is where, you know, um Kevin Stock done an excellent article about um as ALT, the liver enzymes for instance, and and how they can be elevated. Another example here actually Anthony of you know as soon as you understand what let’s get it really basic right if you run and you your legs are worn out you’ll make more enzymes to repair your legs right simple as that so if we had a blood marker was leg enzymes oh it’s up well you were runner yeah right fair enough that was it I mean it’d be that simple so when we look at alt alanine uh transformation which is the which basically is repair is is protein synthesis. So if you’ve got broken uh muscle fibers, which is partly what happens when you exercise, here’s an enzyme that’s critical in producing uh pyuvates and glutamate from other substances which they swap around. So that’s what that’s what the enzyme does. Moves the amino group across, which is where the name comes from. Well, once you know that that’s what it’s doing, it’s making more muscle cells or it’s involved in protein synthesis. Makes total sense that it’s going to be elevated. If you do intensive workouts, simple. So, you know, we can glibly say, “Oh, your ALT is a bit elevated. Do you work out?” Yeah, I work out. Oh, that’s probably all right. But it’s nice to know if someone says, “What does that mean?” But as soon as you, that’s why I like the leg analogy. As soon as you say, that’s basically what happens. Enzymes make stuff and you’ve broken loads of stuff, right? So, you need to rebuild it. And it’s the same. So HBA1C is a marker more of red blood cell viability and lifespan and and health. To be honest, if my HBA1C went right through the roof, but my C peptide, my fasting insulin, my fasted glucose was fantastic or I wore a CGM and I had like you say the flatline, wonderful management, I’d be like, “Wow, my red blood cells are super human. Look at that.” So you could you could completely flip what the usage is and say this is great for your red blood cell life because if you get into you know I I know you could take one thing out of everybody and you know you die if you didn’t have enough this enough that if you take red blood cells out of how you live you know within seconds you’d be gone because it delivers oxygen it delivers iron and and a big thing it does of course is like gases exchange so it takes your oxygen around. Many people miss the fact that when the blood returns to the heart it everyone says de oxygenated. No, it’s saturated with carbon dioxide nutrients. So that you know the the the portal vein portal meaning door you know is the door to your liver coming from every single organ full of nutrients. Absolutely huge amount of blood every minute over a liter of blood full of nutrients full of carbon dioxide and stuff like that. Well that’s the red blood cells. That’s what they’re doing guys. you know, they’re doing everything and we we need to keep them healthy. We need to make sure that we’re not glycating them and we’re not uh damaging the lipid uh portion of the membrane and adding carbohydrates will not do that. It will definitely make uh it would be deletterious to them. Simple as that. Because I’m going to go back to that point, you know, you are glycating and deranging proteins in an irreversible fashion once you put glucose into your system. Even if the superhero insulin is in abundance, you’re not going to stop that level of glycation, that’s that’s going to go up. So when someone says, “Ah, 15 grams of carbs, that’s not going to hurt.” Yeah, it is. So if you look at someone like Saladino, I hate to name names. I love him, right? I really do. But I do think he’s aged. I do think he’s aged in a faster way since he’s been having a lot of carbohydrates. Well, that will be because of things like uh collagen being deranged and the cross links being made and that is what aging is that these things these structures permanently fixed together and your skin looks a bit older than it should you know. So that also explains this way of eating and why people feel you don’t really look your age or you’re reverse aging. That’s a phrase we hear in carnivore ever such a lot. And that’s because we’re keeping the carbs out of our system which the mechanism we’re stopping the glycation. We’re stopping all of that irreversible protein damage happening. And at the red blood cell point of things, you’re del therefore your delivery in two three ways. So albamin is not being deranged. It’s not being glycated. So the delivery of everything 60% of protein in our blood is albamin. That’s not being deranged. the red blood cells like I say um you know talking about iron just then 90% of the iron you’ve got in your body right now is coming from recycled hemoglobin so the recycling of red blood cells is really critical as well and the production of hem which is absolutely at the first stage of hem production ruined by glucose it affects the ALA enzymes all of this stuff is biochemistry that you can look up it’s it’s all factual So he is like a fantastic protein and myoglobin you. So hemoglobin is you know like a a cage really where it has four ions in there and that obviously carries oxygen. Myoglobin which is in the muscle um that is like a cage but it only has one iron in it. So a little bit of oxygen for your for your muscle. Well if you if you if you make the production of that not so good. If you if you make that he the heem part um smaller because you’re restricting the en enzyme at the beginning the stage one then everything else every knock on effect is is is there your iron and your oxygen supply. So when you got the guy with hemocchromattosis now then I I think we should talk about maybe copper as well because that’s underestimated. Um what you’ve done is is you’ve improved the delivery right at a sort of atomic level of iron and oxygen because you’ve given him a diet that’s improved the the health of the red blood cell which is the delivery method of iron and oxygen. So you’ve said to this guy right you know you have got an iron problem uh you know genetic but also you’ve made it worse because the environment around that genetic problem is is is making it you know it’s sort of running against the wind you know swimming upstream against against the current. Well what we’ve done is we’ve turned that all around. So yeah you have that thing you’re not a great swimmer but now the current is is pushing you. It’s behind you. We’ve moved that all around. I’m not very great with off the cuff analogies, but that’s what you’ve done. You know, you’ve you’ve got to the nub of it. The iron delivery and the oxygen delivery, the hem itself, the very structure that does all the work is improved with this way of eating. And and we can prove that we know how he is made. We know how red blood cells are made. And I think they’re the key to everything. Which is why, you know, I think I missed my calling when I did the phbotomy. I should have gone into sort of more advanced hematology because it’s absolutely fascinating when you understand that, you know, iron isn’t just about you eat some red meat, it’s got some hem and it’s going to be going to overload you. Um, which is the most ridiculous thing in the world. And that that’s the other thing, you know, you get you get people with, you know, they’re well-meaning. Oh, now I’m eating red meat. I’ve gone to my naturopath and they said, I’ve got to take tons of vitamin C. And I’m like, well, why? Well, because of iron. I’m like, yeah, but that’s non-heem iron from plants. You need vitamin C for you don’t need it for non-heem. There’s no conversion from non-heem heem and it’s uh for those that don’t know, you need vitamin C feroh reductase. It reducts the heem from Fe3 down to Fe2 plus and um you need vitamin C for that. So, you need a lot less vitamin C. So all this all the advice is well meaning but it’s not got the biochemistry or the background to actually justify why they’re doing it. So vitamin C in that instance would have actually been detrimental because we don’t need that much vitamin C. Scorbic acid can actually have a a problem in the cell when we’re talking about you know iron absorption. And you know an often missed part of the jigsaw is copper because when uh Fe2+ comes out of the cell and it needs to go back to Fe3 you need an enzyme called he hein which is named after he I think the Greek god of iron and fire. Now this enzyme is copper dependent. So if you haven’t got enough copper that Fe2 doesn’t become Fe3 doesn’t get transported and it becomes Fe2 in the bloodstream. and you get reactive oxygen species. You’ve also got seruropplasma also going around which um is again that’s you know copper related and that takes the F3 around the body and also has that enzyatic reaction where it will take Fe2 and knock it down put it back up to Fe3 to be able to transport around in the bloodstream. So I think there’s so many little nuances. Um, everyone talks about copper toxicity, iron overload. Well, actually it’s probably copper deficiency that is causing you to have any iron problems, but the end result you got with the guy with hemocromattosis is I think you’ve ticked all those boxes. There is copper in meat and in the carnivore diet, there’s there’s plenty where it’s pretty much devoid in plants because it’s as that’s been the story of all plants. If there is any copper, it’s all locked up because the plant wants it. Yeah, that’s why it’s there, you know. So, yeah. Sorry, I did a bit of a witch there. Went off went off tangent there. That’s like we all do. That’s fine. No, that was that was great, man. Thank you so much for that. And um uh well, that that was that was really really educational. Absolutely great to get a deep dive in all these things. And I think they’re all very very topical things that that are affecting everybody now because like you said, there’s a lot of myths that are going around. And um but if you if you just look at the people that have just been doing this consistently, you know, like you and I and all the people that have been doing this 20, 30 years, the Inuit who have never not done this um or never, you know, had hadn’t done anything different previously, you know, this is this is just you just eat fatty meat until it stops tasting good. And uh and don’t eat other things. You don’t need other things. You don’t need to game the system. you don’t need to game your numbers. Um, you know, lions don’t check their their bloods and and neither do Inuit. Um, you know, certainly if you have a health condition, then then yeah, you might need to track that. Or if you’re in from a deficient state and you’re trying to catch up on your vitamins and minerals and and certain metabolic issues or or whatever, then there might be something to that. But, you know, generally, if you’re just eating what you’re supposed to eat, your blood work should look the way it’s supposed to work. And, um, so I wouldn’t get too caught up on that. And so it’s import I think that’s good that that we sort of did that that deep dive into that and hopefully put some people’s mind at rest. Um Stephen, thank you so much. Can you tell us uh well any parting thoughts and also just where uh people can find you and follow you and and uh see more of your stuff? Final thoughts? Well, firstly I want to thank you Anthony because it’s always great to speak to you. You’re a very generous person. people that don’t know Anthony, other than what you see on the screen behind the scenes, he’s just as nice and pleasant and hardworking and everything. So, yeah, I could cry almost because it’s really nice to meet a genuine person. No, it is. It is. I mean that from my heart. So, yeah, I’ve really felt for you in the last few months. Uh, and you’ve been greatly missed. Right. Um, and you’re a big supporter. All good. Right. Enough of that. Um, yeah, if you want to contact me, uh, my Substack is the UK carnivore.substack.com substack.com if you want the science. Anthony thought that was a deep dive. It really wasn’t. It’s really superficial. Um, but I’m a great believer in demystifying everything. So, I try to get words and tell you what they mean so you can start making your own uh connections. I do a weekly thing. So, it’s every day, but every week I I get some bloods and uh interpret what it’s saying and why it says that and why that might be important or not important. Um, so that would be the first place to go if you want a written article. If you want to go online, I’ve got a YouTube channel which you can just type in YouTube uh.com coach Stephven. You can also look at Steven Thomas BSC honors. Um, so yeah, YouTube’s pretty good. The school community I I host with Richard is excellent. Low carb school. Or if you want to do a live question and answer, if something’s tweaked your interest and you think, “Oh, I’d like to question that.” although that doesn’t make any sense or the guy’s talking out of his rear end. I want to have an argument. Uh then every Sunday at 7 p.m. here in state control Britain, we do a live question and answer where you can come along and ask me or Richard what you think and that’s completely free. So make sure you come to the channel and subscribe and all that sort of stuff. Make sure you do that for Richard as well. Perfect. We’ll put those links in the description and everybody can can go check you out there. And please do follow uh Stephen his Substack and and all his channels uh because there there’s a lot of great information there and uh yeah well thank you very much Stephen it’s been a pleasure as always really good to see you and thank you so much for taking so much time with all of us. Okay thanks thanks Anthony. Thank you and thank you everyone for joining. Hopefully you enjoyed that and if you did please do like, comment and share with anybody you think would find that valuable. Thank you all very much and we’ll see you next time. Hey guys, thank you very much for taking the time out to listen to what I had to say. If you like it, then please like and subscribe to my YouTube channel and podcast. And if you’re on YouTube, then please hit that little bell and subscribe, and that’ll let you know anytime I have a new video out, which should be every week, if not more. And if you could share this with your friends, that would help me get the word out and let me know that you like what I’m doing. Thanks again, guys.

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