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保罗与心胸外科医生菲利普·奥瓦迪亚（Dr. Philip Ovadia）深入探讨了关于胆固醇、心血管疾病、胰岛素抵抗、饮食与健康之间的复杂关系。

保罗提到他经常遇到一种情况：一些人通过改变饮食习惯，比如采用以动物性食物为主的饮食，避免食用种子油和加工糖，感觉身体更健康，精神状态更好。然而，当他们去做体检时，却发现低密度脂蛋白胆固醇（LDL-C，俗称“坏胆固醇”）水平升高。医生看到这些数据后往往会惊慌失措，警告患者必须停止目前的饮食方式，甚至让他们觉得自己随时可能因为高胆固醇而猝死。保罗对此现象感到困惑，邀请奥瓦迪亚医生来分享他对胆固醇和心血管健康的独特观点。奥瓦迪亚作为一名心胸外科医生，不仅在手术台上修复患者的心脏和血管，还致力于预防工作，试图从根本上减少需要手术的病例。

奥瓦迪亚指出，传统医学界对胆固醇的看法过于简单化，许多医生被灌输了一种观念：所有LDL都是有害的，必须尽可能降低。然而，他认为这种观点忽略了问题的复杂性。心血管疾病不能简单地归结为一个数字（比如LDL水平或载脂蛋白B，即ApoB）。他强调，降低ApoB（一种与LDL和极低密度脂蛋白VLDL相关的蛋白）可能需要使用药物，但这些药物并非没有副作用。奥瓦迪亚坦言，每当他看到患者躺在手术台上，这实际上代表了医疗系统的失败，这些患者本可以通过预防措施避免走到这一步。他希望讨论如何从根本上解决动脉粥样硬化的根源，而不是仅仅依赖药物或手术。

奥瓦迪亚分享了他与保罗在“Maha Ball”活动上初次见面的经历，对能与保罗深入探讨这些话题感到兴奋。保罗提到，他的听众对与心脏病学家或心胸外科医生的对话特别感兴趣，因为这些专业人士直接处理心脏和血管问题。奥瓦迪亚确认自己是一名心胸外科医生，经常进行开胸手术，如冠状动脉旁路移植术，亲手修复患者的动脉和心脏。

随后，保罗引用了一条来自X的帖子，来自一位名叫Gwendolyn的用户。她提到她的丈夫在坚持肉食六个月后，血脂检查结果让医生大为震惊：LDL-C超过350毫克/分升，高密度脂蛋白胆固醇（HDL-C，俗称“好胆固醇”）为62毫克/分升，甘油三酯为90毫克/分升，总胆固醇高达498毫克/分升。医生警告说这些胆固醇数字非常危险。保罗询问奥瓦迪亚对此类情况的看法（明确表示这不是医疗建议）。奥瓦迪亚表示，这种情况在他现在的预防实践中非常常见。他除了做外科手术外，还致力于帮助患者避免需要手术，而高LDL是许多采用低碳水饮食（如肉食或生酮饮食）的人遇到的典型问题。

奥瓦迪亚认为，传统医生对高LDL的反应过于恐慌，因为他们被灌输了“所有LDL都是坏的”的观念。但他强调，LDL是否危险取决于具体情境。仅仅知道总LDL-C的数值远远不够，还需要了解LDL颗粒的大小、患者的胰岛素抵抗情况以及炎症水平等。他指出，真正判断心血管健康的关键不是血脂检查，而是通过影像学检查（如冠状动脉钙化评分，CAC，或CT冠状动脉造影）直接观察心脏血管的动脉粥样硬化情况。CAC评分是一种简单、便宜的检查方式，可以作为起点。如果需要更详细的信息，可以考虑CT冠状动脉造影或Clearly扫描。

保罗分享了自己的经历：他在严格遵循肉食时，LDL-C也曾高达350毫克/分升以上，甘油三酯低于100毫克/分升，HDL-C则较高（75-95毫克/分升，甚至有时超过100）。但当他四年半前开始在饮食中加入碳水后，LDL-C显著下降到130-150毫克/分升。即使如此，他的医生仍认为这个水平偏高。奥瓦迪亚对此表示认同，认为LDL的意义必须结合具体情境来看。他建议检查空腹胰岛素水平（理想值低于8微国际单位/毫升，保罗提到他更倾向于低于5），并通过HOMA-IR或LPIR评分评估胰岛素抵抗。此外，炎症标志物如C反应蛋白（CRP）、铁蛋白、髓过氧化物酶（MPO）等也很重要。奥瓦迪亚还推荐核磁共振（NMR）脂质分析，以了解LDL颗粒的大小和类型，因为大颗粒LDL通常无害，而小而密的LDL和VLDL更具风险。

对话转向了ApoB（载脂蛋白B），近年来医学界越来越强调降低ApoB以预防心血管疾病。奥瓦迪亚对此持怀疑态度，指出ApoB并非单一物质，包括VLDL、小而密LDL（这些可能有害）以及大颗粒LDL（通常无害）。尽管ApoB比LDL-C更能反映某些风险，但仍不足以全面评估心血管健康。他提到，许多知名脂质学家拒绝接受“并非所有LDL都相同”的观点，尽管相关研究早已存在。奥瓦迪亚认为，胰岛素抵抗和炎症是判断LDL是否危险的关键因素，而这些往往被忽视。

保罗提到，西方医学倾向于“一刀切”的治疗方式，例如只要LDL超过120（甚至100）毫克/分升，就建议使用他汀类药物。奥瓦迪亚对此表示赞同，认为这种缺乏个性化的做法忽略了患者的整体健康状况。他还提到，他汀类药物虽然被广泛使用，但存在显著的副作用，包括增加胰岛素抵抗、诱发2型糖尿病、肌肉疼痛以及可能的神经认知障碍（如记忆力下降）。更令人担忧的是，PCSK9抑制剂（一种更强效的降脂药物）在FOURIER试验中显示，尽管降低了心血管死亡率，但总体死亡率（包括感染和癌症导致的死亡）却更高。这表明，过度降低胆固醇可能损害免疫系统功能。

奥瓦迪亚分享了自己的健康转变经历。他曾是一名肥胖的医学生和年轻医生，遵循低脂饮食和热量控制的传统建议，却始终无法维持体重。2016年，他在一次胸外科会议上听到了记者加里·陶布斯（Gary Taubes）的演讲，陶布斯讨论了糖的危害和低碳水饮食的潜力。这启发了奥瓦迪亚，他开始尝试戒糖并采用低碳水饮食，成功减重并改善了健康状况。此后，他进一步转向肉食，体重稳定，健康指标（除LDL外）均显著改善。他的LDL目前在250-300毫克/分升之间，但CAC评分两次检查均为零，表明没有动脉钙化。他还提到，自己的家族有心脏病史，父亲和祖母都曾接受心脏手术，因此他的健康改善显然与饮食和生活方式有关，而非遗传优势。

保罗提到一项由戴夫·费尔德曼（Dave Feldman）领导的研究，探讨了“瘦体超敏者”（lean mass hyper-responders）的胆固醇问题。这些人在采用生酮饮食或肉食后，LDL显著升高（平均273毫克/分升）。费尔德曼的研究比较了这些人与迈阿密心脏研究中LDL较低（平均123毫克/分升）的匹配人群，发现高LDL组的动脉斑块负担并未增加。一年后，研究再次检查了这些人的斑块进展情况，结果显示斑块评分平均保持稳定，LDL和ApoB与斑块进展无相关性。奥瓦迪亚认为，这项研究挑战了“ApoB直接导致动脉粥样硬化”的主流观点，表明LDL的危险性取决于代谢健康状况。

关于胰岛素抵抗，奥瓦迪亚认为这是心血管疾病的首要驱动因素，主要由饮食引起，尤其是加工糖、精制碳水和种子油。他建议通过低碳水饮食（如肉食或生酮饮食）逆转胰岛素抵抗，同时改善睡眠、增加户外活动和减轻压力。保罗提出了一种假说：过量的亚油酸（在种子油中含量较高的欧米伽-6多不饱和脂肪酸）可能是胰岛素抵抗的罪魁祸首。亚油酸可能通过氧化应激和线粒体功能障碍导致能量代谢效率低下，从而诱发胰岛素抵抗。他建议减少猪油、鸡油、橄榄油和牛油果油的摄入，优先选择亚油酸含量低的动物脂肪（如牛油和黄油）。奥瓦迪亚对此表示认同，但指出在实践中完全限制亚油酸可能难以坚持，尤其是在非牧场养殖的猪肉和鸡肉中亚油酸含量较高的情况下。

对话最后，奥瓦迪亚反思了医学界的现状。他指出，尽管心血管疾病仍是全球首要死因，但过去80年来，医学界在对抗心脏病方面几乎没有进展。相反，随着他汀类药物和其他降脂药物的广泛使用，心脏病发病率和死亡率却在上升。他呼吁医生和患者重新审视胰岛素抵抗和炎症的重要性，通过饮食和生活方式干预来预防疾病。奥瓦迪亚还分享了他的目标：通过他的全国远程医疗实践（iFixHearts）和团队，帮助更多人获得基于这些原则的医疗服务，并建立一个医生网络，让患者更容易找到志同道合的医生。

保罗总结道，对话为普通人提供了宝贵的知识，帮助他们理解胆固醇和心血管健康的复杂性，鼓励他们通过饮食和生活方式改善健康。他感谢奥瓦迪亚的分享，表达了未来合作的意愿，以帮助更多人找到合适的医疗资源。

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00:00

One of the most common things I see in my work is people who are getting healthier. They're eating animal-based, avoiding seed oils, processed sugars, and they feel better. And their LDL cholesterol goes up and they go to their doctor and the doctor says, what are you doing? You need to stop what you're doing. Their doctors have made it sound like they are going to drop dead tomorrow. On this week's podcast, I spoke to cardiothoracic surgeon, Dr. Philip Ovadia. He has some different views on cholesterol and statins than most cardiologists. They have been brainwashed that

00:26

all LDL is bad. But I think that the narrative is much more complicated than simply lowering your ApoB. The whole concept that you can reduce heart disease to one number is just foolhardy. There are some pretty significant downsides to lowering your ApoB with medications. Every patient that ends up on my operating table, that was a failure. It was the medical system failure.

00:47

failure. And I think there are better ways to actually fix the root causes of atherosclerosis. We'll get to all of it in the podcast, guys. Enjoy this one. We got to a lot of good stuff. Dr. Philip Ovedia, thanks for coming on the podcast. It is so great. We finally hooked up and got in the same city. So awesome for this conversation. Yeah, I'm excited. I think people will find a lot of value in this. So we first met at the Maha Ball. Yep. But I've

01:11

been familiar with your stuff and been looking forward to talking with you. I think in the past, my audience has found a lot of value for me talking to cardiologists and cardiothoracic practitioners. So you're a cardiothoracic surgeon, right? Correct. So you do the cut the sternum open, coronary artery bypass grafting. Okay. You're in the trenches repairing people's arteries and people's hearts. Exactly. I wanted to start with this tweet that I saw today and we will jump from here. So this is a tweet from Gwendolyn.

01:36

She is saying, “Help, my husband is six months into carnivore, just got his blood work. The MD scared him to death with these cholesterol numbers.” She says the LDL, presumably the LDL-C,

01:48

greater than 350 milligrams per deciliter, HDL 62, triglycerides 90, total 498. So what is your perspective, not medical advice, but what is your perspective on these cholesterol numbers in somebody that's six months into carnivore? Yeah, so this is probably the most common thing I deal with now in my preventative practice.

02:08

practice. So besides being a surgeon, I've been working to keep people off the operating table. And this is the big one, right? Everyone gets this, and I shouldn't say everyone, a lot of people get this hyper responder response when they go on the low carb diet, the LDL goes up, and their conventional doctors freak out because they have been brainwashed that all LDL is bad.

02:34

And really what this question comes down to is, is LDL always bad or is it contextual? And the answer is, as you know, it's context, right? It's the environment that the LDL is in. And you need to know more detail about the LDL. Just knowing the total LDL-C is not enough. You want to look at those particle sizes. You want to look at insulin resistance, inflammation, and T.

03:02

Then the other big piece I think that most conventional doctors miss is

03:08

If we want to know about heart disease, we want to know about atherosclerosis, we got to look for it. And that's not blood work. That's imaging. And that's the other key piece that I put in. Let's look at the blood vessels of the heart if that's what we're ultimately concerned about. So like a clearly scan or a CT coronary angiogram or a CAC. Exactly. Or just start with a CAC scan is a great way to start. You know, simple…

03:32

inexpensive, and we'll start there and then we'll see. Sometimes CT angiography is important, clearly is a great scan. I use it a lot, but I always start with the basics. Let's get a CAC scan. Let's see where you're at. And then let's go from there. Let's break it down a little bit for people. So

03:51

Because I get this question a lot also, and I do broad strokes education now. I don't see patients anymore, but I get a lot of people emailing, DMing, questioning me in person saying something like this. Not even people on carnivore necessarily, right? So I used to be on a carnivore diet. When I was on a strict carnivore diet, my LDL was about like where his was. It was sometimes above 350 milligrams per deciliter, sometimes 330.

04:15

And my triglycerides were usually low, so less than 100, usually less than 80.

04:20

and my HDL was usually quote high, usually 75, 85, 95 even. I think I've had HDLs above 100 in the past on strict keto diets. Now, when I included carbohydrates in my diet, which is something I did about four and a half years ago, my LDL came down a lot. So we're gonna get to Dave Feldman's recent paper. Dave Feldman is an interesting human. I've had him on the podcast a bunch of times. He's an engineer who's advanced this idea of this sort of lean mass hyper-responder phenotype and the idea that when you go

04:47

keto, some people's cholesterol goes pretty high. The LDL does at least. And I saw that. And then I had to change. But even in people for me who are not on ketogenic diets, and I'm not on a ketogenic diet right now, I have 300 plus grams of carbohydrates a day. My LDL is usually 130 to 150 milligrams per deciliter. So even in people like that, they say, my doctor says my LDL is too high. What do I do? And I love your answer. It's contextual.

05:11

So let's, I responded to this comment on X, similarly to the way that you have. I said, what is his insulin, fasting insulin?

05:19

You want it to be less than 5 micro IU per ml. Do you use that threshold too? Is that reasonable? Yeah, maybe I'm a little bit more generous. I'm happy under 8. Okay. And then I get an insulin resistance score of some sort. A HOMA-IR. We either do the HOMA-IR or the LPIR where we look at the C-peptide and you can do an insulin resistance score off of that. So, you know, insulin levels and insulin resistance are important to look at.

05:47

And then inflammation is the other big piece of the puzzle for me. You want to check that C-reactive protein. You want to see what the ferritin is. I like some vascular-specific inflammation markers. Myeloperoxidase, MPO, is my big one. I'll check LP-PLA2, although when we really want to get into the weeds, we can talk about why that might not be a good marker in some situations. Okay.

06:11

and get the whole picture. And then, like I said, you got to get that NMR panel. You got to see what your particle sizes are. And like you said, this isn't really about the hyper responders. This isn't really about, you know, ketogenic diets, low carb diets. It's understanding what LDL tells us and what it doesn't tell us. And, you know, the whole concept that

06:39

you can reduce heart disease to one number is just foolhardy, right? This is a complex, you know, complex disease state. It has lots of things that influence it. And, you know, I just kind of shake my head thinking, how in medicine did we think that this one number was going to tell us everything we needed to know about heart disease? You know, I was a PA in cardiology before I went to medical school.

07:05

And that we were myopic. You know, when I was working with cardiologists, they were very intelligent, well-intentioned people. And they literally would mime to me, think here, right? Think in the heart box.

07:18

And if there was an LDL above 120, that person goes on a statin. And now it's even almost above 100 for a lot of people. And there are these guidelines. And again, I've heard you say this, and I really appreciate it. A lot of this is more contextual than people believe it is. And Western medicine seems to me to want to treat it as one size fits all. And that just doesn't seem to be the case. But right now there is a growing, I think it's grown a lot, but there is a growing trend

07:44

fear or sort of zeitgeist around ApoB, which is similar to LDL-C, as low as possible. What do you think of this? Yeah, you know, it's the same problem, right? Because ApoB is not one thing, right? ApoB is VLDL. ApoB is small, dense LDL. Those things are problematic. But ApoB is also large LDL, which is not problematic. So once again,

08:11

ApoB is better than LDL because it does account for that VLDL, but it still doesn't give us the full story. And I've gone round and round with many of the, we'll say, leading lipidologists, right? Many of the MD, big name MDs out there about this. And for whatever reason, they just won't accept this concept anymore.

08:36

even though it's in the studies, it's in their literature, right, that not all LDL is the same. And when you look at things like insulin resistance and inflammation, it predicts, it tells you who LDL is problematic for and who it isn't. And like you said, it's just easier, right, to make blanket statements. Treat everyone's LDL, keep it low,

09:01

And, you know, that might be okay if it didn't come with the side effects. Exactly. And there are side effects of the medications. There are side effects of the dietary changes that were suggested to lower LDL. We see, you know, low-fat diets. They've been a disaster. They make people more obese. They make people more insulin resistant. And so we have to take that into account. And this…

09:28

What I really come back to is this, and, you know, I got a few more gray hairs than you, but we were doing things about the same time, right? And so, you know, I did my training, graduated medical school in 1998.

09:41

I did my training, you know, to be a general surgeon first. And then I was deciding what area of surgery I wanted to specialize in. And I just loved cardiac surgery. I love the technical aspects of it. I love the physiology of it, understanding how the heart works. And so, you know, this is 2001, 2002. I'm talking to my mentors and I say, I want to go into cardiac surgery. And they said,

10:08

Don't do it. You're crazy. There's going to be nothing for you to do in 20 years. We have these medications. We've figured out heart disease. Heart disease is going to go away and you're not going to have anything to do.

10:23

And needless to say, here we are 25 years later. I am busier than ever. There is a critical shortage of heart surgeons in this country. There are not enough heart surgeons to go around and do the heart surgery that needs to be done.

10:38

And you step back and you say, why is that? And you can say, okay, we don't train enough surgeons or the training to become a heart surgeon is too brutal, which it is. It seemed brutal to me from the outside. Yeah. But the real problem is, why are there so many sick people? Why do so many people need heart surgery? And that's the question that

11:01

I started asking about a decade ago as I went through my own personal health transformation and now I just look around me and I'm still in there. I'm still doing the surgery but I'm looking around and I realize that every patient that ends up on my operating table, that was a failure.

11:19

And it wasn't the patient's failure. It was the medical system failure. These patients, most of the time, have been seeing cardiologists for decades. They've been on these medications. They've been following the advice. And it failed them. And we need to ask that question more. Why? Why are they here? It's the type of question that wasn't asked when I was in medical school.

11:45

We never asked it when I was working in cardiology as a PA. It's just, it's a broad failure of the medical system, I think. It's just the paradigm is wrong.

11:53

The medical system is not set up to ask these questions, whether it's, why does this person have eczema? I had eczema growing up, right? Why does this person have asthma? Why does this child have autism? Why does this person have cancer? Why does this person have cardiovascular disease or lupus or Sjogren's or osteoarthritis? We are taught, here's the medication. Here's the medication. Here's the medication. That's what we do as doctors. And I think it's just a broad failure in terms of the ethos of medicine. And I completely agree with you.

12:19

I want to get to some of the details of the things we were talking about earlier, but I want to hear a little more of your story. You, when you were in your training,

12:28

You were much more obese than you are today. You've lost a lot of weight. Yep. Tell me about that. Yeah, so my training, my early career, really up until about 10 years ago, I was morbidly obese. I was pre-diabetic, right? I had reached a point where I knew that I was headed for my own operating table, so to speak. I was looking at my patients and looking at me and saying, you know, we're on the same path.

12:56

And I also understood that I didn't know what to do about it because I was following the advice that I was giving them, right? Eat your low fat diet, count your calories, you know, food pyramid, all that stuff. And it wasn't working for me. It wasn't working for them.

13:14

And, you know, thankfully, really, I started to come across some different information. It really kind of crystallized for me. 2016, January, I'm at a meeting of the Society of Thoracic Surgeons. So this is all heart and chest surgeons. And there happened to be a guest lecturer by the name of Gary Taubes.

13:39

And I'm sitting in this room with a thousand, you know, plus surgeons. And honestly, I'm thinking, why are we listening to a journalist? You know, like, what does this have to do with anything, right? He's not going to teach me how to do heart surgery better. But, you know, I was open enough to listen. And, you know, that was right when he had written the case against Sugar. And he was talking about, you know, everything Gary talks about. And it clicked. And I said, okay.

14:08

This sounds like it could work. Let me try it. I cut sugar out of my diet, went on a low carb diet, had great results. And then I started looking into it more, started realizing what this had to do with the disease process that I had dedicated my career to. And also realizing and asking, why didn't I hear this from my mentors? Why didn't I hear this from, you know, my colleagues?

14:35

And again, no offense to Gary, and I've told this to him, you know, personally, but why did I learn about this from a journalist? And, you know, that literally changed my personal life, my professional life. And here we are now, you know, coming up on a decade later. So you tried eat less, move more. You were trying calorie restriction, diet.

14:59

exercising, and it didn't work for you. Yeah, you know, I would have the brief success like lots of people, right? I remember, for instance, my chief year, so the last year of my general surgery training, and I said,

15:12

I got to lose weight, right? I got to get under control. This was right when the Palm Pilot had come out, if you remember, right? One of the first sort of smartphone-ish type devices. And so I was able to download a program, tracked everything I ate. We had a gym right attached to the hospital. So between cases, I'd be going to work out, really did it as best as you could do it.

15:38

And yeah, I lost, you know, probably 40, 50 pounds that year. But within a year, I had gained it all back and more. And that was probably the, you know, third time I had gone through that cycle in my life, right? And I was only, you know, in my late 20s at this point.

15:55

And, you know, again, it's what people have experienced. You can do it for the short term, but you can't do it for the long term, literally because you're just trying to starve yourself and, you know, your body rebels, right? Your body needs nutrients. It needs nutrition. And when you're depleting yourself like that, you reach a critical point where your body says no more. And as a survival mechanism, you get more hungry. And that's the bottom line.

16:24

And when I did it this way, right, when I cut out sugar, went low carb, I wasn't hungry because I was still getting the nutrients that I needed, right? Plenty of animal protein at first, you know, vegetables and some fruit, although I later cut those out when I went more carnivore. But even on carnivore, right, you're getting the nutrients that you need and you're not

16:49

depleting yourself. You're not starving yourself. You're not hungry. And so it is sustainable and it does work in the long run. And again, here I am nine years later now and the weight has stayed off and my health is better by every measure, except maybe one. Which one? Yeah, maybe that LDL, right? Right, true, fair. But yeah, everything else looks great.

17:15

What is your LDL now? My LDL runs between 250 and 300. My CAC score checked twice, three years apart, has remained zero. Zero. And that's in the context, right? Everyone says, oh, well, maybe you have great genetics. No. My dad died of heart disease. My dad had bypass surgery. My grandmother had heart surgery.

17:36

I have two siblings who both have non-zero scores, we'll say. And so it's clearly not genetics working in my favor. It's what I'm doing. It's the diet. It's the lifestyle. And, you know, again,

17:54

I have personal stake in the game, right, when I'm talking to patients about what does high LDL mean and what doesn't it mean, because I'm living it as well. What about fasting insulin and your other inflammatory markers, if you may ask? Yeah. So, fasting insulin runs between four and six. CRP always very low, less than one. All the other stuff looks good. I'm not quite

18:19

lean mass right my uh but my triglycerides usually run around 70 and my hdl is in the mid 50s to lower 60s uh so you know it's it's good i think by my you know by the standards i use and i'm metabolically healthy you're a metabolically that's the key thing and i don't have inflammation and i

18:41

The LDL is not problematic, right? And my particles are large and pattern A, all of those things that we can look at. I want to pause the podcast just for one minute to tell you guys about something I'm really proud of. I built Heart and Soil about four and a half years ago. We make desiccated organs. We put them in capsules. In this podcast, you've heard Dr. Ovadia and I talk about heart, but one of my favorites is Whole Package. This has testicle, liver, and blood in it. And a lot of men find a ton of benefits with Whole Package.

19:08

There's a women's supplement called Her Package. We make lots of desiccated organ capsules that also contain heart. If you want to get heart or other organs into your diet without actually eating the organs. Like I said in the podcast, I have been known to put raw heart in my smoothies. But if you don't want to do that, check us out. We have grass-fed, grass-finished organs in gelatin capsules. All of our stuff is in glass. You can find us at heartandsoil.co. We'll circle back to some of these things we talked about at the beginning of the podcast. You said you have a CAC scan.

19:35

A CAC is what I did. I did it about five years ago. Mine was also zero when I was 42. I also have a family history of early onset heart disease and a primary relative. My father had an angioplasty when he was 42. My CAC was zero with a LDL cholesterol of 350 plus at that time in my life. And that was about when I switched to eating carbohydrates. My LDL is much lower.

20:00

And that's interesting. The downsides as far as CAC goes, as I can tell, is it has more radiation, right? So if people are thinking, what are they going to do for imaging? You have CAC, CT coronary angio. I guess these all have some radiation, right?

20:14

So is this something to think about? Is it safe to get a CAC every year? How much radiation in a CAC scan? One millisievert? Yeah, it's pretty low. It's about equivalent to a chest X-ray. Oh, it's that low? Yeah, it is that low now. And it's about how much radiation you're going to get with like an average flight, right? Across the country? Not even across the country. A couple hour flight, you know,

20:37

The amount of excess radiation that you're exposed to during that is going to be equivalent. So there's really no reason not to get it. Yeah, I do think you can get a CAC every year. I don't think it's necessary every year for everyone. What I tell people is, you know, if you have a zero score, depending on your age, you know, you can wait three, maybe five years to check it again. If it's non-zero, I think…

21:03

I know that the CAC is a great way to follow progression, right? Because again, it's that low radiation, it's inexpensive. And so I do like to get it every year until we find that things stabilize, right? And that's my goal with patients. If your CAC score isn't zero, and if we've ruled out real bad disease, severe disease, and we'll talk about that next, you know, I just want to keep that CAC score stable.

21:31

Everyone always asks, can I make it better? Can it go down? And yes, you can. I've seen that, right? I've seen it go down 10%, 15%, 20%. Not going to go from 200% to zero, but if you're 200%,

21:45

And next year, you're 200 again. Great. If you're 175, 150, probably even better. The honest truth is we don't have a lot of studies on that because it doesn't happen a lot with the traditional approach. But we do have very good studies that show that as long as it's not getting worse, as long as it's not progressing, and the average progression in the studies, you know,

22:11

you know, not looking at this type of population. When you just look across the population, on average, it goes up somewhere between 15 and 20, maybe 25% per year. Okay. Most people. So I tell people if it's going up less than 5%, which is sort of the margin of error of measurement anyway, we're doing good. You're at low risk of a cardiac event and what you're doing is working. And if it's not,

22:41

Then we have to figure out why. And that's an important thing. You know, we can't just assume that if you're doing a good low-carb carnivore diet that you can put your head in the sand and ignore it, right? Yeah, yeah, we'll talk about that. Yeah, exactly. There are people that continue to progress. There might be many reasons for that, but you got to pay attention to it. Yeah, yeah. Even if you're doing an animal-based diet and you're eating carbohydrates, I mean, I think that, like we talked about, the goal is just to be insulin sensitive. That's the major context. Metabolic health, I think, is king. Yeah.

23:10

And giving that context, ApoB is something that I think is important in the conversation. It's starting to be talked about more. So the CAC, the coronary artery calcium score only tells us calcified plaque. And then the clearly in the CT angio can tell us non-calcified plaque? Correct. It's going to give you non-calcified plaque. It's going to give you percent blockage of the blood vessels, right? This is the other thing you don't get from the CAC. And they don't

23:38

Track linearly, I'll say. I've seen people with CAC scores maybe as low as 200 that end up having significant blockages. We need to put a stent. We need to do bypass, something like that. I've also seen people with CAC scores in the multiple thousands that didn't need a stent or didn't need bypass.

23:58

So, you know, the CAC score isn't the end-all and be-all. It's a screening test. It's a great way to follow progression, like I said. But, you know, depending on your situation, you might want to get that more detailed CT angiogram. Now, the drawbacks of the CT angiogram are it is more radiation. It's more expensive. So that's something I reserve, you

24:25

you know, I don't necessarily want to be getting that every year on people. And depending on the situation, we work it in, right? I use the CAC first. The CT angiogram becomes the more detailed test that really tells you what's going on in those blood vessels. I think most people can get a CAC score even without a doctor's prescription these days.

24:46

I think you can get it just on your own. It's like $200. It's not even that much. And you know, a CT coronary angio is probably 2000 plus. So you're going to need a doctor's prescription. You're probably going to want your insurance to pay for that or, you know, get some other stuff going on. But a CAC is pretty accessible these days. It's almost like a

25:00

It's almost as easy to get as a DEXA in a lot of places. Yeah, exactly. And yeah, same thing that you said. You don't always need a doctor's prescription. Sometimes you do. It's going to depend on the imaging center. So technically, you do need a doctor's order for it. But a lot of these imaging centers have their doctor that will order it for you. So you don't need your doctor. Yeah.

25:23

And I've seen it as cheap as about $59. 200 is actually the high end. They're very reasonable tests to get. The CT angiogram, again, more involved.

25:39

The price is coming down. I've seen cash pay prices for these things now around 500 bucks. But going up to 2000, you need the doctor's order. Your heart rate needs to be slow enough when they do the test. So you might need to take a medication to slow your heart rate for the test. And then they're going to put an IV in. They're going to give you contrast through the IV test.

26:03

There's a small risk of, you know, problems with the contrast, but that's very small. So it's still a very reasonable test. And in a lot of situations, insurance will cover it. So it may not cost you anything out of pocket, you know, depending on your situation. But like I said, it's not my go-to right off the bat. Get the CAC first. Yeah. So I think a lot of people, I want people to know that you can get

26:26

The labs that we mentioned, all these labs are available without a doctor's prescription now. There are third-party websites now that have their doctors on staff. You can get a fasting insulin, an HSCRP, myeloperoxidase, fasting glucose to calculate a HOMA-IR. You can get a lipid panel. You can even get an

26:45

NMR lipid panel, everything we've mentioned so far, you can do without even going to see your doctor these days. And I do it all the time. I mean, when I come to the States, I'll go to one of these blood work places. I have no affiliation with any of them online and I'll order my own blood work. You just need someone to help you interpret it. But I think that the, I'm excited that the barrier to these is lower than it used to be for people. So you can do your own cardiac evaluation and

27:10

Obviously, I think working with a doctor like you or someone else that's knowledgeable is important, but I don't want people to think that there's a barrier to these things. And then if you need to, you can go to like a CT coronary angiogram or a ClearlyScan to get more information. And so this is probably a good segue to Dave's study. Before we do that, I forgot I have gifts for you. So I don't know if you've had breakfast today, but I got you some lineage meat sticks. We've got, this is our new collagen. I got you some…

27:40

testicle capsules. All right. Do you eat testicle? Uh, I do now. I have not eaten them yet. Um, I,

27:48

I am a big fan of the organs. Ironically enough, heart is my favorite organ to eat. Heart is amazing. I love it. You know, kind of like a nice lean steak. But I'll definitely give the whole package a try. Yeah, let me know what you think of these things. And at the end of the podcast, I'll have you try a meat stick to let me know what you think of that. Because these have organs in them too. Love it. And yeah, guys, just so you know, this is our new collagen from Lineage. It's exciting. It's exciting.

28:13

for me because it has hyaluronic acid and multiple types of collagen, trachea, scapula. You guys will hear about it. That's the cool stuff. So,

28:20

I think heart is another organ that I'm excited about because of the coenzyme Q10 in it. So I've done something recently. I don't tell people about this too often because it's a little bit gross, but I will take raw heart and put it in my smoothie and just blend it up. So I make a smoothie in the morning now of raw milk, honey, blueberries, creatine from lineage. I've got some lineage honey and maybe some collagen from lineage and I'll put in some raw heart and

28:44

in there and it just blends up and I just drink this raw heart. But I mean, we'll get to statins later in this podcast and the downsides of a statin, but I just think humans getting

28:53

preformed coenzyme Q10. It's in muscle meat, but it's very rich in heart. So what an amazing thing to be eating. Yeah, definitely one of the densest sources of it that we can eat. And I agree with you. I think it's, you know, it's great for your heart. It's great for your mitochondria in general. And unfortunately, it's one of those things that is

29:13

is oftentimes deplete in people. They're not getting enough of it because they've been scared away from eating even muscle meat, you know, let alone something like organ meat. And so it is a common deficiency that people have. And especially if you have heart disease, it's a problem. It's one of the essential factors

29:32

uh kind of uh supplements or nutrients you know that i recommend getting a lot of for people with heart disease and i think people can just eat meat it's it's you know i would not even i mean maybe you feel differently i wouldn't even recommend people supplement because

29:46

I've checked my Coenzyme Q10 levels, which is another thing you can get over the counter, and they're always off the charts. They're always, and that's just like, to me, it makes so much sense. Why would something like red meat that is full of myriad nutrients, right? Whether it's creatine or carnitine or answering or taurine or Coenzyme Q10 be bad for us? Like if you just eat more red meat and heart, your Coenzyme Q10 will go through the roof and that's better than any supplement you're going to get on Amazon, right?

30:11

it just makes so much sense to me. Diet is so much simpler than it's made out to be because I think we've lost the plot. But yeah, I mean, do you ever check your coins on Q10 levels? I actually have never checked my level. I'd be curious. You got to check and let me know. Next lab work, I'll get it. Yeah, I get it. One of the other things pointing out, like you said earlier, how accessible it is, right? Getting that lab panel that we just talked about

30:34

It's going to cost you $200, maybe $250 to do that. So again, not a huge barrier. And the unfortunate thing I see over and over, right? People come to me, people message me on social media, and they're like, my doctor won't order this for me. Right. Right. And you might say, well, why? And the reality is, is that the doctors won't order it because they don't know what to do with it.

30:59

They don't understand that information. It's not part of the algorithm, right? You know, we didn't learn about, you know, the stuff in medical school. And so unless you've taken that initiative as a doctor to really go learn this on your own, uh,

31:14

You don't understand what the tests are, so you don't want to order it and then be kind of staring at them and the patient's asking you about it and you're like, I don't know what to do about this. So it's kind of one of the screens that I tell people to use to figure out, is your doctor knowledgeable about this stuff? Are they going to be able to work with you on this stuff? Ask them about those types of tests and see what they say.

31:40

Let's talk about Dave's paper because this is exciting. Today is April the 11th. This paper came out four days ago. Dave Feldman, like I said, guys, has been on the podcast multiple times in the past. We had talked about the first phase of his study,

31:52

where he looked at the plaque score of his cohort of lean mass hyper-responders and compared it to a matched cohort of the Miami Heart Study. So the first phase of this study Dave talked about on the podcast, and it showed that his cohort of lean mass hyper-responders with an average LDL of, I think, 273 milligrams per deciliter did not have more plaque burden compared to an age-matched cohort from Miami Heart that had an average LDL of 123. That's interesting.

32:19

And when they did the regression analysis, there was actually no correlation between plaque score and ApoB in his cohort.

32:28

So what's exciting about this paper he just published is this is the analysis one year later. The original intent of his study was to take lean mass hyper-responders, people who are on ketogenic, sometimes carnivore, sometimes not diets, and have very high LDLs. Like I said, the average LDL is over 270. To get an original CT coronary angiogram. They may have used clearly, specifically, I forget. Yeah. And then to do it one year later and to look at plaque progression because…

32:53

I mean, maybe I think you could speak to this better than I can, but my impression is that most people in the lipid space would say, if your LDL is around 300, you should see plaque progression in a year if ApoB is really driving heart disease.

33:06

independently. And so I'll let you talk about it, but I think it's an incredible study. Yeah. The patients that come to me oftentimes, you know, with those types of LDL levels, right? Their doctors have made it sound like they are going to drop dead tomorrow, right? Yes. Go to the hospital now. Yeah. You got to do something about this. And here we now have data to show that one year later, like you said,

33:30

with this exposure to the high LDL levels. And important to point out that in order to get into this study, you had to have been on the diet for at least three years before the initial scan, right? So now for the second scan, you're on at least four years of this diet. You've had this increased LDL for that time. And so you're right. We would expect if LDL was what it's purported to be, that we should see significant improvement

33:58

progression of plaque during this time, and they didn't. On average, the plaque scores were flat. Important to note that there were some people in that study that did go up. There were a few that went down, and most stayed the same when you look at the data. Again, when they did this regression analysis and they looked at the factors that predicted

34:29

Did your plaque go up during the year? LDL and ApoB had no relationship to whether or not your plaque increased. And the only thing that they found that had a relationship was how much plaque you had on the first scan. That's interesting. And so the people that had more plaque on the first scan were the ones that tended to go up more during the year. And I think that is interesting, right? And, um,

34:54

And it might be a caution, right? Again, because maybe not all lean mass hyper-responders are the same either. And if you're a lean mass hyper-responder with more plaque to start with, maybe there is reason to be concerned. Now, the things that I've thought about, and I haven't had a chance to talk to Dave or Nick yet about it, but what came to mind when I was going through this study is,

35:19

there's probably something more about why those people had plaque, more plaque to start with. - There's something missing. - Right? There's something we're missing. And, you know, again, this is what I think about in my practice every day, because when I do have patients, right, we know these people were not insulin resistant. We know they had low inflammation. Those were,

35:41

And maybe you could say they, you know, the entry criteria, right, were that you, CRP was one of the entry criteria. It had to be, I think, below two, maybe below one. I don't remember exactly, but I think below two to get into the study. So they kind of ruled out inflammation. They monitored ketones and they looked at insulin levels. Now,

36:05

there may be insulin resistance, right? This is one thing that, um, at least in the data that's in the study, isn't entirely clear. Like, are we sure that these people aren't insulin resistant? And, you know,

36:22

the audience, right, people might be thinking, wait, they've been on a low-carb ketogenic carnivore type diet, right, for at least three years. How could they still be insulin resistant? And I can tell you, you can still be insulin resistant. Wow, okay, you've seen it. I've seen it, right? We're dealing with people, the average age of the people in the study was 55, right? So four to five years on a ketogenic diet.

36:47

50 years of not on a ketogenic diet for most of them. And, you know, that insulin resistance can take a long time to recover. Some people, by the time they've started the ketogenic diet, they already have such advanced and severe insulin resistance that they can't reverse it completely. So, again, this is where you really got to get into the numbers. You know, even fasting insulin can…

37:16

be a little tricky, right? Because when you go back to Dr. Kraft's original work, right? He was kind of the one that described insulin resistance. And you think about those patterns. If you remember, there's the five patterns of your Kraft test, right? So the Kraft test is you drink a whole lot of sugar, 75 grams of sugar, and you look at your insulin response and you look at your glucose response. And

37:43

And there are some people that start with a normal low fasting insulin level, but they have this delayed insulin response. It's either pattern two or three. I can't remember which one that is. But so you can have a normal fasting insulin level and still be insulin resistant.

38:02

So that's, again, why I check things like LPIR scores or HOMA-IR. So, again, I don't think that was fully, you know, worked out there. They didn't get fasting insulin on the people. And I've talked to Dave about this. He said they still have frozen blood, but they didn't. I said, Dave, you didn't look at fasting insulin. I'm dying. And I even commented on his post on X, and I said—

38:26

Let me help you fund, you know, with the Animal-Based Nutrition Research Foundation, the nonprofit that I created. I want to fund the next arm of the study or the next secondary analysis going back and looking at the blood and saying, okay, in the people where there was plaque progression, which were the people, those were the people who had the most plaque, like, are they more insulin resistant? Can we see a pattern in fasting glucose?

38:48

fasting insulin and HOMA-IR, which is just a calculation with the fasting glucose and the fasting insulin. But I would love to go back and do that. The other thing I want to see is thyroid levels, because that's the one thing that I've seen in some people on keto and carnivores. The thyroid gets a little wonky, and I wonder if that could be affecting things in there too. And again, this is a unique population,

39:09

that's on a ketogenic carnivore diet. That's why the LDL goes so high, which makes them interesting to study. But yeah, there's a few unanswered questions here, but the takeaway was pretty strong for me that, look, if the mainstream high priests of lipidology are correct, an ApoB causes atherosclerosis,

39:31

How does that happen? How is there zero correlation between ApoB and plaque in these humans? Like this is not the case. It's obviously contextual. And I haven't seen Tom Dayspring or Peter Attia respond to this at all. I have a call with Peter next week for a debate that I'm doing

39:49

on seed oils on his podcast later this month. And I'm going to ask him about the study and we'll see what he says. He might just deny it. He might not even comment on it, but it's, you know, it's funny because I've, I've never directly connected with Peter and I have respect for him, but I think he's dodged things like this. And I think that there's, there's a lot of, there's a lot of, you know, I would say, uh,

40:09

non-consistent data points in the space with lipids that make me think, if ApoB really directly caused atherosclerosis, then why do we see findings like this? Why do we see, you know, secondary analyses of things like Framingham or other studies that show that when you stratify by any variable that approximates insulin resistance, the relationship between LDL and cardiovascular disease is massively attenuated. And, you know, the ApoB causes atherosclerosis camp doesn't want to

40:37

talk about that and I don't get it. So it's just, it's a little bit strange to me. Yeah. So, you know, as yesterday, I recorded a podcast episode with Gary Taubes. And one of the things we talked about was,

40:50

you know, what are the mistakes that are made in science in general, right? And nutritional science might be one of the worst examples, but, you know, ignoring the negative evidence, right? Ignoring what contradicts what you believe is probably the worst mistake you can make in science, right? The whole point of science is to disprove what you believe, right?

41:13

And it's only after you try to do that multiple times and can't that you then accept your hypothesis. And the lipid hypothesis has so many holes in it. And again, it's in their literature, right? And one of the favorite recent studies I point to was looking at PCSK9 inhibitors, right? These are the most powerful lipid-lowering agents we have.

41:40

The patients on these medications oftentimes will have LDL levels in the single digits, in the teens, incredibly low LDL levels, right? And when you go back to the main trial that led to their approval, it was called the Fourier trial, and they did the sub-analysis, and they looked at patients'

42:01

based on their metabolic risk factors, right? How many of the five metabolic risk factors did they have? And the patients that did not have metabolic syndrome, zero, one, or two of the metabolic risk factors did not get any benefit from lowering their cholesterol. So

42:21

That's the answer, right? It's there. And that's not the only analysis like that, right? There's another PCSK9 trial that I'm aware of with a similar analysis. There are loads of statin trials where they've selected out, right, something that approximates insulin resistance. And honestly, I've never seen a study that truly does this well, like pulls out the truly insulin sensitive people, because to be honest, there aren't a lot of them around.

42:50

But, you know, even if you approximate it, right, something as broad as having normal blood glucose levels, you lose the benefits of cholesterol lowering. So the answer is there. They just don't want to look at it. They don't want to. And I don't know why. It continues to amaze me. I think that…

43:14

Western medicine doesn't do a good job of nuance, right? We want to treat all patients the same. And we want to have guidelines. And if those guidelines are too complicated, physicians who are overworked

43:28

and not given enough time with their patients would really struggle to, I think, to make the decisions easily. And that would be very hard for doctors. And you see this at every level of medicine, whether it's pediatrics or geriatrics or internal medicine, there are blanket guidelines that say, hey, I mean,

43:44

When a baby is born in the hospital, the first thing they do, obviously, is a hep B vaccine and a vitamin K shot. I don't, you know, like, I don't think all babies born in the hospital are vitamin K deficient because, you know, I mean, I think some might be because the moms are not eating enough animal products and maybe they're going to get hemorrhagic disease of the newborn. But do all infants need a vitamin K shot? No, but it's standard, but they don't check levels in mom. It's too complicated, you know, and do some infants benefit from a hep B shot at birth because the the

44:12

mothers never bring the baby back to the hospital? Possibly. But do we really need to give hep B to an infant, you know, that hep B is obtained from IV drug use or, you know, prostitution? Like, these are strange things that we do in medicine. And medicine doesn't appreciate nuance and context very well. And so I see this with lipids also. And this is what worries me because

44:33

Like you said, like we started on the podcast, a lot of people change their diet. They get healthier with their diet. And if they listen to you or they listen to me, they might just eat a few more hamburgers without the bun. They're going to get rid of seed oils. They might eat a steak, right? Three or four times a week or maybe every day. And a lot of these people are going to see their LDL go up. Sometimes it's 10 to 20% like it is in me. Sometimes it's 200% if they're doing more keto or low carb, if that's what works for them.

44:59

And then they're doing great. They go to their doctor and the doctor says, you got to stop what you're doing. And he said, well, doc, I'm losing weight. I feel great. I have more libido, more energy. No, you got to stop because it's all I see. I think so much of Western medicine lives and dies on the cholesterol, the lipid hypothesis. It's like, it's like this fundamental piece of the house of cards. And it makes sense. I mean, statins are a huge, huge part of our pharmaceutical industry. And I'm not saying that pharmaceutical companies necessarily are conspiring against us, but

45:25

Sometimes it looks a little strange to me. And I think that the way that we treat statins is a little bit interesting. And I think there's a lot of questions about statins that we'll get to, but it doesn't add up to me either, right? It doesn't add up. We're saying, why are we doing this to patients? If you have a patient coming to you and they're insulin sensitive, like you said, most doctors aren't even checking these markers. We're just going on one myopic marker. We're treating everyone the same. And it hurts some people, I think, to do that. So let's talk about the flip side, right?

45:53

Because people always come to me and talk about this compelling case, admittedly, that's been made from lowering ApoB. Because, you know, cardiovascular disease is the number one killer in the world today. And you can decrease your rate of cardiovascular disease by lowering ApoB. Why would we not want to lower ApoB? What are the downsides of potentially lowering cholesterol? Because if I can die of cardiovascular disease less, like, I'm going to push it as low as I can.

46:18

Yeah, and again, that question doesn't get asked, but we have some concerning evidence here again. And again, I'll go back to the FOREA trial, the PCSK9 inhibitors, the most powerful cholesterol-lowering medication we have. And in that trial, and all the patients in this trial were on statins, and they either had PCSK9 inhibitors added or they were in the placebo group. They didn't get PCSK9 inhibitors added.

46:44

and more patients overall died in the group that got the PCSK9 inhibitors. And, you know, that's really not something you can argue with, right? There is some controversy around the FOREA trial because the claim was that there were less cardiovascular deaths in the group that got the PCSK9 inhibitors. That's what led to their approval. Now, there was an independent group that was able to reanalyze that data and

47:12

And they came to a different conclusion. They felt that the deaths were misclassified, whether or not they were cardiovascular in both groups. And when they reanalyzed everything, they felt there was no difference in cardiovascular deaths. But, you know, you can't argue if someone is dead or not. So there were still more deaths in the group that got the medication. And that's a big red flag, and it should be a big red flag.

47:37

And I don't think any doctors know this, right? These doctors prescribing the PCSK9 inhibitors, they don't know about it. They didn't hear about it, right? In the paper, it was downplayed. It didn't reach statistical significance. Now, the trial was stopped early. And if the trial had gone to the full five years that was planned, maybe that difference would have been statistically significant. But, you know,

48:03

There's good reason, right? Because when you look at that, you say, okay, well, what were those excess deaths from? They were from infection and cancer. And it makes total sense because we know what cholesterol does in our body. It is part of our immune system. It's a vital part of our immune system. And so lowering it to that degree might have issues.

48:25

What other issues do we worry about with cholesterol lowering? Certainly with the statins, not clear I would say with the PCSK9 inhibitors.

48:35

After you've been on statins for more than five years, there is an increase in insulin resistance. And insulin resistance is the primary driver of heart disease. The very thing we're trying to fix. Exactly. So what are we doing here? There are more patients with type 2 diabetes after being on statins, and that's very concerning. Cholesterol, very important to our brain. And the incidence of neurocognitive disorders, memory loss,

49:02

concerning as well, right? And I admit not definitively proven. The literature is, you know, kind of mixed, but there's at least that concern. There are the short-term symptoms that many people hear about, right? The muscle aches and those types of things.

49:16

Memory issues. Yeah, memory issues in the short term, right? So like we said, if the intervention had no side effects, then yeah, go ahead, do it for everyone, right? But we don't have any interventions that don't have any side effects, and we need to consider these side effects. And when you're looking at these studies that have number needed to treat

49:38

around 80 or 100, right? So only one out of every 80 patients is gonna benefit from taking that medication. And there's some potential harm

49:49

And ultimately, listen, the patient should be the one making the choice, but they need that information. And they don't get that information. Most doctors, again, don't even know this information to be able to give it to the patients. But these are the questions that we need to do a better job of asking, you know.

50:10

What is the true benefit of taking this? What are the risks of taking this? And then, you know, in my context, right, for me, and this is the difference between studies and individuals. And as physicians, you know, we have to remember our duty is to that individual in front of us. It's not to the healthcare system. It's not to the population at large, right? It's that individual in front of you. You need to figure out with them what is best for them.

50:39

I appreciate that so much because I think that these frank conversations are not being had. And again, they're complicated. I don't think as doctors we're trained to have conversations like that. I don't think we understand the data well enough to have those conversations. And I think that there is some degree of fear in the population on heart disease.

50:59

No one wants to die of a heart attack. Somehow dying of cancer seems like it's further off, but heart attack is a strike, right? You get, oh, I stopped breathing or you just fall over dead. Maybe we all know someone who's tragically died of a massive sudden heart attack or a cardiac arrest, and that seems scarier, but ultimately we all just want to live the longest lives possible as well as possible. And if an intervention decreases my risk of heart attack or

51:25

or cardiovascular disease, but increases my risk of suicide or cancer or a immune-related death. It's all the same in the end. And, you know, I've heard many people, Dave Feldman included in this, argue that why are we looking at cardiovascular mortality

51:41

Only we should be looking at all-cause mortality in every single study. And if a statin or a PCSK9 inhibitor or any medication does not improve all-cause mortality consistently, we need to be asking some serious questions. Because if we're just shifting the death toll over to cancer and infectious disease, that may make it look good from a cardiovascular disease perspective. And, oh, we're just going to end the trial early.

52:05

And maybe these won't be, we're just kind of sweeping these things under the rug. But we have to remember that these are complex biological systems. Let's talk about statins a little more again, because you brought this up and it's very important. I think it illustrates this point. Statins inhibit an enzyme in the liver, HMG-CoA reductase, which is part of this Mevalonate pathway, this cholesterol synthesis pathway.

52:25

But also in that pathway downstream from cholesterol is coenzyme Q10. And we talked about this with heart. Coenzyme Q10 is a key portion of the electron transport chain in the mitochondria. So I don't think it's very surprising that statins could increase insulin resistance because they're negatively affecting our ability to make energy in the mitochondria. And ultimately, I think insulin resistance is important.

52:51

mitochondrial failure. And that term gets thrown around a lot. But if we really distill, and let me know if you agree with this, if we really distill mitochondrial dysfunction, what is that? I think that's failure of adequate or efficient energy production at the level of mitochondria. So anything you do, you or I do, that negatively affects my mitochondria is likely going to make me more insulin resistant. Taking something that blocks the formation of coenzyme Q10 in your body is probably going to make you more insulin resistant. It's going to give you the very thing that you're trying to fix. That

53:19

That's crazy. All right, one more pausing the podcast, guys. I am so proud of these things that I've built. I want to tell you about lineage. You guys know about lineage provisions. We make grass-fed, grass-finished meat sticks with organs. These have heart and liver in them. We talked about heart a lot in this podcast with Dr. Avadia. And our newest product is our collagen. But this is not any collagen. This is our nose-to-tail collagen. What makes it

53:39

better. It's grass-fed, grass-finished bovine collagen plus trachea and scapula cartilage. So it has collagen types 1, 2, and 3. We also include eggshell membrane, which has naturally occurring hyaluronic acid and elastin, which help with skin elasticity and hydration. We included acerola berries for naturally occurring vitamin C and salt. So I'm really proud of this collagen. I wanted to make the best collagen on the market, the most bioavailable collagen, the highest quality collagen, and I think we did it. Check out our nose-to-tail collagen at lineageprovisions.com. Back to the podcast.

54:08

Yeah, no, I agree completely. The whole concept is crazy. And then the fact that it could say, okay, well, you know, you can mitigate that, right? You could supplement with CoQ10. You could tell people to eat more steak, right? Eat some heart, right?

54:25

And that's not even done, right? It's actually discouraged, right? You ask the standard cardiologist, well, why don't you give CoQ10 with your statins at least? Maybe that will mitigate some of the side effects. And they believe that not to be helpful. And again, it's crazy why there are some studies that were done that were in

54:48

I won't say intentionally, but they appear to be intentionally designed to be lousy studies, right? Doing things like giving too low a dose of CoQ10, not measuring CoQ10 levels and, you know, being too short. And, you know, and then they say, oh, look, there's no benefit to this. So why would we? And I think the reason is, right, because if you admit that problem.

55:10

Then you have to, you open up that can of worms of, well, why are we poisoning our mitochondria intentionally? It's a big deal. Yeah. Other things that poison the mitochondria, just so people know, metformin.

55:23

and berberine, both complex one, at least partially inhibiting. So I think we have to be careful with those. But yeah, there are a lot of things that we do in our lives that sort of poison the mitochondria. Most of them are things that are very poisonous, like cyanide, you know. But we do things in our lives that are poisonous to the mitochondria and harmful. I think sugar being one of them, and we can talk about why, probably through lipopolysaccharide. But yeah, you do not want to poison your mitochondria and statins

55:49

pretty clearly look to be doing that. And as I've heard you say on other podcasts or in one of your videos on your YouTube channel, the full data for statins has not really been made available to the public. It's kind of like it's siloed in this like British, like halls of…

56:04

Harry Potter Hogwarts. Where is it hidden? There's a guy, one of the main guys involved in the statin research, I forget his name, he's knighted in England and he's in charge of all this statin data. It's never been released to the public. It's in a horcrux somewhere. What is going on? That in and of itself is crazy. And

56:22

And, you know, more problematic to me these days, right, is so now people are starting to say, okay, well, we have other options for lowering cholesterol pharmaceutically, right? We have these PCSK9 inhibitors. We have ezetimibe. We have benpidoic acid. So, well, okay, maybe we should shift to using those more. But they still skip over the first part of the question, right?

56:47

Is cholesterol lowering beneficial? Right? And again, like we've said many times, the data is pretty clear. If you don't have insulin resistance and you don't have inflammation, cholesterol lowering has never been shown to be beneficial. I don't care what method you use, diet or any of the pharmaceuticals. And so,

57:08

Oftentimes, I'm bringing people back to that question first, right? Because we oftentimes have this discussion around the statins like you and I just had, and then they say, oh, okay. And then they go back to their family doctor, and their family doctor says, well, take azetamide. Right.

57:23

or go on a PCSK9 inhibitor. And I'm like, I mean, literally, like, you know, right before we started this podcast, I was messaging with one of my patients about this because, you know, we had had a meeting and we said, okay, you don't need the statins. And then they went to their PCP and the PCP said, well, if you don't want to take statins, take a zetamide. And it's like, no, cholesterol lowering is not beneficial. So we find ourselves just, and again, we're, we're,

57:51

We're like, I kind of think of it as like Don Quixote, right? We're trying to fight this imaginary, you know, enemy that never existed in the first place, right? Cholesterol was never the enemy. Never the bad guy. And somehow we're in this battle to now prove that is not bad when it was never proven to be bad in the first place. And I think that there probably are some people in whom cholesterol lowering is indicated.

58:19

If they, I mean, I would imagine, and maybe you agree with this, if someone is absolutely insulin resistant and is not going to change their diet, okay, isn't there, there is a conversation that maybe these medications are indicated in some places. But for most of the people listening to this podcast, I think there's a big question about whether they're actually beneficial and why.

58:41

What I see as the most important first step, at least in terms of broad medicine, is we should be checking insulin resistance and inflammation in any patient that we're even considering prescribing a lipid-lowering therapy to and asking them,

58:54

are you willing to change your diet? Are you willing to sleep better, get some sun, go outside? But then I think we get to the $64,000 question, which is what causes insulin resistance? And we should probably talk about that a little bit too, because when I got out of medical school, I don't even know if I'd heard the term insulin resistance. I think I heard the term metabolic syndrome and I knew the criteria, low HDL, right? High blood pressure, waist circumference, et cetera, et cetera. But

59:21

It's never talked about in medical school, at least when I went to medical school. I kind of want to go back into hospitals and just say, do you ever ask patients about insulin sensitivity or do you think about this? But I think that more and more doctors are waking up to the fact that this is metabolic health. And so from your perspective, if it's all about insulin resistance and inflammation, and let's just talk about insulin resistance first,

59:41

How do we fix insulin resistance? How do we get to… Because that's probably the real root cause here, right? Exactly. All right. And so, you know, again, what causes it, right? If you don't know what causes it, you really don't have a good chance of fixing it. And so insulin resistance is…

59:59

I'm going to say almost exclusively diet related, right? First and foremost. There are other factors that come into play. Of course, activity, sleep, you know, stress, sunlight, all of these things are important, but diet first. And, you know, it's things in our diet that are clearly causing insulin resistance. Insulin resistance, you know,

01:00:23

We can imply. We don't really know because we haven't had the testing for it for an extended period of time. Again, Dr. Kraft did his work, 70s, 80s. Before that, we really didn't know what insulin resistance was or have a good way to test for it. But it's clearly increased more.

01:00:44

more recently in our history, and it correlates to a number of possibly harmful things in the diet, right? And, you know, I mean, in our community, of course, the big debate is, is it sugar and processed carbohydrates? Is it vegetable and seed oils? Is it both?

01:01:04

And the true answer is we don't know that for sure, but they both have good evidence. They both have good mechanisms to suggest that they're contributing to insulin resistance. So in my mind, the answer does become sort of simple. Eliminate them both as much as possible, right? And the processed carbohydrates, the processed sugars, the vegetable and seed oils, these things clearly aren't essential to the human diet, right?

01:01:33

they are strongly associated with and have mechanistic explanations for why they cause insulin resistance. So let's get rid of them first. I think the sugar conversation is more clear cut than the seed oil conversation. When I look at sugar,

01:01:51

And feel free to add to this if you disagree. But when I look at sugar, I'm not convinced that insulin-induced insulin resistance is the main mechanism, but I am interested in this dysbiosis mechanism with processed sugar. When I dug into this, I thought it was pretty fascinating. I tweeted about this on X, that when you give a human sucrose,

01:02:09

pure glucose, pure fructose, we really do see changes in the gut microbiome that result in increased endotoxin, increased LPS, lipopolysaccharide, which is a component of the gram-negative cell wall.

01:02:21

And there are other endotoxins, but this is the main one, is lipopolysaccharide. And there's pretty good evidence that when you have endotoxemia, when you have increased levels of endotoxin in your blood, your body mounts an inflammatory response and your mitochondria kind of shut down. So I think the data is pretty clear cut, at least mechanistically. And there are some intervention studies that show this. If you feed a human sucrose, endotoxin goes up. I think that's a pretty clear mechanism that if you give someone pure sugar,

01:02:47

And the toxin goes through the roof because of dysbiosis. Now, what's interesting for me about this, and then I'll get your take on it, is that fruit doesn't seem to do the same thing because of all the other compounds in the fruit that prevent dysbiosis. And we've seen this. Like, you can give someone fruit, you don't get overgrowth of bacteria in the gut because there's sucrose, which is glucose and fructose, but then there's also 500 other compounds, which are actually kind of just affecting the gut microbiome in a way that they don't get out of control. That's really interesting to me, and it kind of makes sense

01:03:14

from a historical evolutionary perspective. So what do you think about that? Do you think fruit is harmful for humans or processed sugar versus fruit? What's the balance here? - Yeah, you know, I think fruit can be harmful if you're already insulin resistant, right? When you're insulin resistant, you cannot process carbohydrates and sugar properly, no matter what source it's coming from. Now, if you're not insulin resistant,

01:03:39

No, I don't think fruit is going to cause you to become insulin resistant. Too much processed sugar certainly will. I think it will. Yeah. I think that if, I think I'm insulin sensitive and I eat a lot of fruit and honey, you know, um, partial to lineage honey these days. If, and I, I mean, I eat

01:03:59

150 grams of honey a day. My fasting insulin is three, you know, and my fasting glucose is 74. And I would do a, you know, I would do an insulin tolerance test or any test. I'm pretty sure I'm insulin sensitive. So in myself and many other people, I've seen this, but I'm pretty sure that if I ate sugar, equivalent amount of spoonful, yeah.

01:04:19

and this is the counter-reductionist perspective, that over time I would change my gut flora or I would increase the lipopolysaccharide, that I might become less insulin sensitive. And I think that probably would happen for me. Yeah, I think so too. And, you know, the thing that sort of complicates the discussion, right, is no one's sitting there eating, you know, bowls of

01:04:40

straight sugar. Unless you're eating Frosted Flakes, but yeah. Well, even, yeah, I mean, but most of the time, so the problem with our food environment is most of the time,

01:04:51

where that sugar is coming from in the diet has vegetable and seed oil. You know, has other processed ingredients in it, right? So it becomes very difficult to really separate out the effects of, you know, what is the sugar itself doing, right? And on the other side of things, the vegetable and seed oil discussion, right? No one really sits there and guzzles canola. It's in these processed foods with the sugar, right? And all the other stuff in it. And so, um,

01:05:20

That is the challenge from a scientific standpoint. But again, from a practical standpoint, the answer is very simple. Get rid of the processed food. You're getting rid of all of that stuff.

01:05:31

you know, have your animal proteins. And like I said, if you're insulin sensitive and you want to put some fruit in, you want to have some, you know, kind of vegetables, right? And you're going to get some carbs from them. Fine. I don't think it's a big problem. I always tell people carnivore isn't the only option.

01:05:56

But I want people to understand it is an option, right? And this is the other kind of battle we have is that the

01:06:04

this concept that eating red meat is bad for your heart is causing cancer, you know, all of this stuff, none of which again was ever true, but that's what we have to battle against. So the main message I try to get to people is eat real food. Um, the more insulin resistant you are, the lower carb it needs to be to be able to reverse that. And then, uh, you know, like I said, if you want to include some fruit, some veggies, uh,

01:06:34

And you're kind of staying within your limits. And this is where tools like a continuous glucose monitor can be great to help you figure out what your limits are. I think that's a very reasonable way to go about things. You can reverse your insulin resistance. You can lower inflammation, which is the other thing, you know, that comes into play. And

01:06:56

you can live a nice, healthy life like that. I think it's all about reversing insulin resistance. I think most people that are listening to this podcast who are insulin sensitive are probably savvy enough to stay that way, you know? But I think that the real people that we need to help are those to reverse insulin resistance. And I think the steps are pretty clear. I agree with you on most of that stuff. I think if you're eating processed sugar, you got to get rid of it. And I think if you're eating seed oils, you

01:07:20

even just from a historical perspective, get rid of them. It doesn't make sense. And we can talk about some mechanisms in a moment. And then I think, yeah, if you're very insulin resistant, you're not going to tolerate carbohydrates well, so it's reasonable to lower them. I don't think personally that they got you there, but your machinery is kind of broken, so you should maybe limit them somewhat. And then you can increase them if you want in the future as you become more insulin sensitive.

01:07:43

Can I share with you a little theory that I have? I've talked about this on a few podcasts, but I want to get your take on this. So one of the things that I think gets neglected in the keto and carnivore communities is the idea of absolute amounts of linoleic acid. And this is connected with the seed oil conversation because I've been thinking about seed oils a lot. Like I said, I'm preparing for a debate on Peter Atiyah's podcast later this year on seed oils.

01:08:03

And mechanistically, I am concerned that excess linoleic acid per se, which is this 18 carbon omega-6 polyunsaturated fat, which is predominant in seed oils, anywhere from 25 to 55% from canola to soybean oil or other oils. I think this mechanistically might be harmful for humans when it gets to be too much. And I think that's the main problem with seed oils is that they have lots of linoleic acid. They're a very cheap, easy way to just stuff your body full of linoleic acid.

01:08:32

What we know about human physiology is we accumulate these polyantestrogen. They get stuck in our body. But what's interesting in this, I got pushed back when I've talked about it in the keto and carnivore communities in the past, but I think I keep coming back to this idea that I don't see many people talking about, because if the goal is to reverse insulin resistance, and if we find the mechanism of excess linoleic acid compelling,

01:08:53

because of oxidative liability, you know, you fill all of the membranes of your body with linoleic acid, the mitochondrial membranes, the cell membranes, and that both creates proton leak at the mitochondria between the inner membrane and the matrix space. And in the cell membrane, there's

01:09:08

there's leak of probably electrolytes, sodium and potassium, causing over-utilization of the sodium-potassium pump. So from a whole energy perspective, linoleic acid looks to be very bad. And when we're not producing energy efficiently, we become insulin resistant. It's sort of this cell danger response, or at least a reactive response in the cell saying, hey, we're not making energy well. Like we don't need any more energy. We're backing up.

01:09:29

if we can't move electrons through the electron transport chain efficiently and make ATP, the cell does tend to accumulate metabolites that say, I want to become insulin resistant. Insulin resistance is a response to poor energy production. And I think that linoleic acid clearly impairs our ability to make energy at those molecular levels.

01:09:46

Now, I think that my hypothesis is that in your practice and other people's practices, if we're not attending, if we're not paying attention to the overall amount of linoleic acid in our diet, we're not fixing the insulin resistance fast enough. Because conventional eggs have a lot of linoleic acid. Pork fat has a lot of linoleic acid. Chicken fat has a lot of linoleic acid. Olive oil, avocado oil have moderate amounts of linoleic acid. I mean, so…

01:10:13

Wild chickens, 4%, 5% linoleic acid in their fat. Conventionally raised chickens, 20. Olive oil, 15, 20% linoleic acid. Not a seed oil, not industrially processed, but still lots of linoleic acid. Things that we would never have really been doing historically as humans 200,000 years ago, even up until 50 or 20,000 years ago, we didn't have much of these oils in our diets. And

01:10:37

for any of these cultures that were olive oil heavy, Mediterranean cultures, they haven't had seed oils before the last 100 years either. So yeah, if your ancestors are Greek and they were using olive oil, great. The highest oil in their diet was 20% and it wasn't refined, bleached, and deodorized. And they never had any soybean oil and they never had any of these other sources of linoleic acid. So,

01:10:57

I guess what I'm wondering is, could we get people healthier faster from an insulin resistance perspective if we recommended overall linoleic acid limitation and said, you might actually want to limit pork fat

01:11:09

You might want to limit lard. You might want to limit olive oil and avocado oil. You might actually want to limit, eat like chicken fat. And I thought, oh, that's kind of interesting. But it's, these foods are sort of sacrosanct, right? It's sacred to say, you can't take away my bacon. I'm on a ketogenic diet. The whole reason I'm eating ketogenic is I want to eat bacon. I'm thinking, I'm not sure the bacon is good for you. Now, I don't think bacon is going to make you or I insulin resistant, but in somebody that's already potentially not doing energy metabolism well,

01:11:37

Don't you want to like limit the amount of linoleic acid so we can recycle the membranes as quickly as possible? What do you think about this idea? It's just a hypothesis I'm sort of working with. Yeah, no, I think it's very valid. And linoleic acid in high amounts is clearly problematic. And lowering it, I think, is a great strategy.

01:11:57

from a practical standpoint, you get into this, you know, if you're restricting people too much, right, that they can't adhere to it. Fair. And, but I think it's very valid. Now, I've seen plenty of people reverse their insulin resistance eating, you know, a lot of bacon. So it's work, you've seen it work, okay. I mean, it can work, but you're right, it might work better if they weren't, you know, eating all that bacon. Yeah.

01:12:25

And, you know, I do talk to people about sourcing, right? And, you know, in the end, you know, because you get into the grass-fed versus grain-fed beef part of it.

01:12:37

And I explained to people that that difference is relatively small, right? It's your non-ruminant animal sources that you really want to be paying attention to. And unfortunately, they're more difficult to source, right? Grass-fed beef has become kind of common now. You can find it. A good pasture-raised pork or chicken or eggs, like you said, is almost impossible to find. So I think it's very valid. Yeah.

01:13:05

Like I said, I do worry about the practicalities and making this sort of too hard for people to do. I'd love our food environment to change it, you know, so that linoleic acid isn't as prevalent. Because ultimately, right, if you're cutting out the vegetable and seed oils and the processed food, you're lowering your linoleic acid level a significant amount. You are. You know, but you're right.

01:13:31

you are still getting probably higher than ideal amounts of it, uh, in the, um, in the pork, in the chicken. Uh, and it's another thing that I'd love to see studied better, right? Yeah. We have, we, we have pretty easy ways to measure these things these days, right? You can do, uh, at home testing for your fatty acid profile, uh,

01:13:54

And I think that's a pretty good test. And, you know, generally I do use it some. It's not part of my routine panel in my practice, but I do have some patients that like to track that over time. And generally when people are on, you know, we'll call it a more broad ketogenic diet, they're

01:14:13

Their levels are decreasing. Of linoleic acid. Of linoleic acid. But you're right. We probably could decrease them quicker, and that would likely lead to quicker healing, quicker recovery from insulin resistance if we really focused on it. Or in some of your patients…

01:14:30

that are difficult to reverse their insulin resistance. I just wonder, would that be an adjunctive therapy that's just a dietary intervention? So yeah, I like to put it out there. I've talked about it a few times in recent podcasts. I hope some of the people listening to this podcast

01:14:43

who may be struggling with continued obesity or insulin resistance despite dietary changes, might consider it. And the prescription, for lack of a better word, is really just to shift your fats. You know, tallow and butter are 2%, 1.5% to 2% linoleic acid. They're very low compared to olive oil and avocado oil. Olive and avocado, I think, are better than seed oils.

01:15:07

unquestionably. Choosing an olive oil is tricky. Choosing an avocado oil is probably even more difficult. I don't love that most, quote, healthy alternatives today have the olive and avocado oils. And when you go out to eat, it's almost always avocado and olive oil now. It's a better choice, but it's, I don't know that it's ideal. But butter and tallow are not liquid at room temperature, so I'm not sure how most places are going to cook. You can't put butter on your salad.

01:15:31

I don't know why people are eating salads in the first place. Skip the salad. That's the answer. That's a whole separate conversation. But I do wonder, just hypothetically…

01:15:41

in humans who are struggling to reverse the insulin resistance or want to do it more quickly, if you switched all of your fats to animal fats, which again is just apostasy, but it's very controversial and I think it would be radical, and you limited chicken and pork and you focused on beef or ruminants in general, which would be lamb, elk, bison, beef, cow, et cetera, you would significantly reduce your linoleic acid very quickly. And I wonder what that would do to us metabolically because

01:16:08

When I do the analysis of like my fatty acids, it says my linoleic acid is like lower. It's like below, they're like, well, your linoleic acid is lower than it should be. And I'm like, I feel pretty good. You know, I don't think it's a problem. And obviously it's all, the reference ranges are based on some sort of Gaussian curve of the population. So I've fallen probably two standard deviations outside of the mean now in terms of how low my linoleic acid is.

01:16:33

and I feel great and I don't really have to work very hard to stay lean. And I wonder if that sort of a shift could help other people with this question because ultimately it just all comes back. The mechanism is fascinating to me. Mechanistic ideas won't win a debate on seed oils, but there is really a mechanism there. It's just, it's much harder for the body to control polyunsaturated fats from an oxidative perspective than it is monounsaturated or saturated fats. And that just creates more work

01:17:00

And we know, similarly to the lipopolysaccharide, that when you have oxidative stress, when we have reactive oxygen species, that is lipid peroxides, lipid peroxide radicals being formed from linoleic acid, that can shut down the mitochondria too because it's a signal. Reactive oxygen species are made by the mitochondria. This is our life, is the movement of electrons. If we

01:17:19

If we have too many of these sparks flying out of the fireplace and the living room starts to catch on fire, the mitochondria are just like, get out the fire extinguishers and shut the whole process down so we don't burn the house down. It makes so much sense to me mechanistically. I'm always trying to think like, how could we show this in a study? And the other problem with seed oils is

01:17:37

before we move on is just that all of the randomized control trials were done 60 years ago. Yeah. 50 to 70 years ago. And none of them are great. None of them are great, but don't forget that again, the baseline assumption is that they're good for you, right? They have the American Heart Association stamp of approval on them. They lower your LDL, right? So they must be good. Uh,

01:17:58

And so it's a very uphill battle. But again, hopefully the environment is changing, right? And we haven't gotten into the whole, you know, maha yet. But, you know, like we said, you and I met, first time we met in person was at the ball. And we're starting at least to have these conversations, which is great. And I think more and more people are becoming aware of this, which is great. And

01:18:26

Ultimately, again, high level.

01:18:29

Get rid of the processed food. I think first and foremost, that's the thing that you need to do to improve health if you're, you know, on the sort of standard Western diet. And, you know, in the end, now we're talking about the nuance, right? Oftentimes, you know, this is the difference between the, you know, doing very well and trying to make things perfect.

01:18:57

And so when you're working with patients, sometimes you have to compromise. Sure. And I think that's reasonable. But ultimately, yeah, I don't see any benefit to having large amounts of linoleic acid in the diet. I think we should be trying to eliminate it wherever possible.

01:19:18

The history around this is fascinating to me. I've heard you mention this and it's so striking. I think it really illustrates the point for people. 125 years ago, 1900, the turn of the century, 99 plus percent of the fats we ate were animal fats. Tallow, butter, lard.

01:19:33

What were heart disease rates 125 years ago?

01:19:52

And that's really the most mind-blowing thing, right? And going back to the kind of broad discussion around physicians, one of the conversations I have with my colleagues these days is just, are we happy with the results that we're getting, right? It's a very basic question. Like,

01:20:12

you know, why is heart disease still the number one killer? Yeah. We declared war on heart disease. You know, this is something interesting as I was going through the history, right? Many people point to 1955 and President Eisenhower, you know, has his heart attack in office and that's the beginning. It turns out that 1949 is when the government first declared

01:20:36

declared war on heart disease, right? It goes back before that even. So again, here we are, we're coming up on 80 years later, and the problem has gotten worse consistently, right? We have not made any progress against this. When you look at the curve of heart disease deaths, right, there was a little bit of an improvement from about 1990 to about

01:21:03

early 2000s, 2005, you see a little bit of a decrease. That is probably attributed to the decrease in smoking during that time. And since 2005, it's been back up, right? And it's at its peak levels. I mean, we have made zero progress. And so, you know, that's the biggest failure, right? That's what everyone should be shouting about. You know, you talk about

01:21:31

you know, doge that's going on, right? And wasted money. The trillions of dollars at this point that have been pumped into fighting heart disease and we have gotten nothing for it. And that's what's most amazing to me. The number of people, like you said earlier in the podcast, more people are probably on statins and PCSK9 and Bempadoica. We are treating, pharmaceutically lowering LDL more than we ever have in history.

01:21:58

I mean, that's a pretty strong statement. I think that's a pretty accurate statement. And heart disease incidence is higher than ever? Is that fair to say? So the incidence is higher than ever, despite more LDL lowering than ever before. Okay. And then you're saying that heart disease deaths, so the mortality from heart disease is also the highest it's ever been? What are we doing? We're clearly doing something wrong. And…

01:22:20

I mean, I have a friend on Twitter who says like, how many, you know, if seed oils are so great for us, like how many seed oils do we have to eat? You know, we're eating the most seed oils, you know. It's the same with statins. Like how many statins do we have to take? Like statins are so good for us. They're going to lower ApoB. We're going to really stop dying from, you know, heart disease. How much…

01:22:40

How low do we have to push LDL? Like how many seed oils do we have to eat and how low do we have to push LDL before we start seeing people actually, you know, live longer or, you know, have less heart disease? It's crazy. Clearly we've got the equation all wrong. This is interesting to me. You mentioned when you have conversations with your colleagues, what is it like having conversations with your colleagues? Do you have colleagues that feel the same way as you or not?

01:23:02

Is it difficult to hold this perspective? Because I agree with you. I'm not in cardiology anymore, but you have a radical perspective based on Western medicine. What's it like?

01:23:12

Yeah, there is some progress I see, right? There are more and more colleagues that are opening their eyes to this, right? I actually know, I'm going to say a moderate amount of physicians now. Really? That do things like low carbohydrate diets for themselves. However, they won't talk to their patients about it. They're still fearful, right? Because it goes against the dogma, it goes against, you know, the guidelines. So, you know, that happens.

01:23:42

I've given a number of grand rounds to, you know, cardiologists. And the way that I usually start the conversation is clearly what we're doing isn't working.

01:23:53

So let's look, what are we missing, right? And this is where you can bring in insulin resistance. Because instead of arguing about, you know, the statins and the cholesterol, and is it meaningless, right? You know how it is. If you go and attack someone right away and say, you're wrong about this, that's not going to lead to a very fruitful conversation. So what I like to do is say, what else can we, should we be looking at? And I bring up insulin resistance. And you know what?

01:24:22

They receive that pretty well. They understand it. Now, again, there are systemic problems. Ordering an insulin level in most hospitals is nearly impossible. I know it's crazy, right? And you ask doctors about it and they're like, oh, that's such an expensive test. I'm like,

01:24:43

You can literally go to some of those sites we talked about earlier, right, to order your own test and you can get an insulin level for $8. And they're like, no, that can't be right, right? And you go into the hospital computer system and you try and order an insulin level and it's like flagged as like a, you know, expensive test and it can't be done. And so there are like these barriers to it, right?

01:25:06

And why that is, we can speculate, but it's a problem.

01:25:15

Like you said, most doctors, insulin resistance was maybe a term they heard during the second year biochemistry course, right? And never heard again. And it doesn't get talked about. We don't know how to manage it. Now, this is where there's sort of an interesting shift going on because we have these new miracle medications, right? The GLP-1 inhibitors. Oh my God. Yeah, yeah. And-

01:25:39

one of the things they do is they actually help with insulin resistance, right? So we also have the SGLT2 inhibitors. And these are another class of diabetic, originally developed for diabetes, but now indicated for treatment of heart disease, heart failure in particular. They also help with insulin resistance. So this is how you can start to bring this into the conversation. You say, you know, you guys are actually unintentionally

01:26:08

treating insulin resistance. Let's talk about it. Let's focus on it. Here's a better way to treat it, right? Instead of giving you these medications, you can just stop eating the carbohydrates. And, you know, that kind of discussion is actually fairly well received. But

01:26:26

But again, it's not happening widely. It's still a vast minority of physicians that ever even hear about this to consider it. And then if the physicians don't hear about it, their patients aren't going to hear about it. So, you know, at times I'm very optimistic because certainly outside

01:26:46

our community has grown. The number of physicians in our community is growing. The number of patients that are interested in this is growing. We have Bobby Kennedy and them talking about it. But then I also realize we're still a drop in the bucket. And all

01:27:05

All we can do is keep talking about it. We just got to get that groundswell. And then that can lead to things like changing the food environment, right? Coming up with, you know, so that 95% of the supermarket isn't filled with

01:27:21

foods that are going to destroy, you know, going to cause more insulin resistance, raise your linoleic acid level, all of that stuff. Yeah. It's pretty crazy. When I was at this, the Maha event, the inauguration, I talked to Chris Palmer and I said, Chris, like, I want to debate somebody at Harvard. Like, let's make it happen. And he was like, oh, I don't know. Like, but like, I want to, I want to debate Walter Willett or somebody from TH Chan about seed oils or insulin. You know, it's just,

01:27:47

Where do we have like where where can we have the conversation that people will pay attention to it in a way? Because I think that these it's just so frustrating for me because, you know, the social media outlets, they've gotten maybe a little better. But they just whenever I do a post about seed oils in the last year, again, it's maybe a little better now, but they would just fact check it. And they would refer to Walter Willett, who would cite a meta analysis from Darius Mazzafarian, who was actually at the Maha things.

01:28:10

But in the meta-analysis that Darius has done from Tufts on seed oils, he's included multiple trials that are complete baloney, right? That should not be included. They're not really double-blind. They're not really randomized. And they certainly are multivariable trials. They're horrible seed oils trials. So it's like, who's fact-checking the fact-checkers? And the whole thing is just this house of cards, you know,

01:28:30

shell game to me. It's super frustrating. And I didn't see him there because I wanted to walk straight up to Darius and say, like, all right, let's go. You know, like, you and I need to get on a podcast and I want to ask you, like, why did you include these trials in your meta-analysis? But I think most people…

01:28:43

are never going to go that deep with the research. They're not going to read, you know, Mazzafarian's meta-analysis and look at his forest plot and go, why did you include the Finnish mental hospital study? You know, that's a baloney trial, you know, and why is this trial in there? And, you know… And why'd you exclude all the ones that don't show, you know, that show that there's no benefit to these? Yeah, why did you exclude, you know, the rose corn oil trial? It's just, the whole thing is kind of rigged to me. So I think ultimately…

01:29:09

Podcasts like this help people because it's just grassroots. People educate themselves. And the good news is that the solution is quite simple.

01:29:17

Ultimately, I think if it comes from bottom up and top down, that's better. If physicians are educating their patients and saying, hey, you have insulin resistance, here's how you fix it with diet, which is the ultimate fix for insulin resistance, that's great. But I think for the last decade or so, people have been getting the information, podcasts like this, and people have been fixing it themselves and then going to their doctor and saying, look at me.

01:29:39

And that's why I think that the lipid conversation is so important because they go, look at me, I'm healthier. And the doctors freak out about LDL. So thank you for coming on the podcast and talking about this because I think it's going to help a lot of people feel better

01:29:50

better and answer questions for them about this lipids, which are often this massive hurdle. People are getting healthier. And then like you said, like yourself, the LDL goes up. What do we do? Well, hopefully this has given people tools. Where can people find more of your work or reach out to you or connect with you? Yeah, definitely. iFixHearts everywhere. So all the social medias, I'm at iFixHearts. You can go to ifixhearts.com. I have a nationwide telemedicine practice. Great. We see people

01:30:18

everywhere, even internationally. Uh, and that's honestly another challenge in all of this, you know, finding the doctors. Yeah. How do people find that? Yeah. It's hard. Uh, and, uh, you know, like I said, I've, I've built a great team. I have a nurse practitioner, three health coaches that work with me and we're, we're trying to make this accessible. Uh, and ultimately, you know, my, uh,

01:30:45

dream, my goal, right, is to make this easy for people. You know, can we build out a physician network that's based on these principles and make it easy for people to find the care that they need? Because, you know,

01:31:00

Ultimately, this is scary stuff, right? Like you said, everyone's worried, am I going to have a heart attack, right? And statistically, it's the number one killer. It's the most likely thing you're going to die from, so you should be worried about heart disease. And there's just so much…

01:31:17

of the other narrative out there. How do we get people who are concerned about heart disease to find this information? Uh, that's sort of the big problem that I'm working on. Uh, but like I said, in the meantime, ifxhearts.com, come see how my team, uh, works with people. And, uh,

01:31:35

We just got to keep working together to spread this information. Well, I appreciate that. It's awesome you have a nationwide telemedicine practice because that'll help a lot of people. And yeah, let me know offline. We can talk about how we can collaborate. Because I've been thinking throughout this conversation, how do we create some sort of a network

01:31:51

to help people find these doctors. And I remember when we, when I founded Heart and Soil five years ago, we had a page and I think the page has since, you know, become mothballed, but we had a page of animal-based, you know, health practitioners. And I think we need to, at Heart and Soil, sort of re-imagine that and re, you know, rebirth that, recreate that. Because I think a lot of people are going to come away from podcasts like this and say, okay, great.

01:32:13

And I want a doctor to guide me. Where do I find people who are thinking this way? So let's, yeah, let me know if I can help you create that. I think that would be really meaningful and helpful for people. Amazing. We'll do it. Thank you for coming on the podcast. Appreciate your work. Great to be here.

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Edit:2025.05.09

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