And he got a little flack for this it sounds like in his medical training, which is really interesting, and we'll get into that. But he also has specific interests in weight loss and in lipidology. And he's not the typical low-carb person. In fact, he is frequently thought of as anti-low-carb, but as you'll hear in our discussion today, he really has an open mind and that's one of the reasons why I wanted him on this show.
Because it's good to get different perspectives. He's going to give you a different perspective on lipids than you hear in the low-carb community. He's going to give you a different perspective about calories and insulin and the carbohydrate model than you usually get in the low-carb circles. But he also has an open mind and he realizes there's a place for different treatments and different tools, and that's one of the things I hope you'll appreciate about him.
Not all of you may agree with everything he says, but I hope you'll appreciate his approach. And more importantly, he's interested in learning more and he wants to help foster more studies so we can learn more about LDL and hyper responders and is it a problem or is it not. Because we can talk hypothetically all we want. What we need is that data and Dr. Nadolsky is someone who's trying to be on that frontline to help us get there.
So, I hope you enjoy this exploration of some different ideas, and I hope you enjoy Dr. Nadolsky's open mind and his approach. So, sit back and enjoy this interview, and if you want to learn more, you can go to DietDoctor.com, you can see the full transcripts, and of course access all the different information we have on DietDoctor.com. Dr. Spencer Nadolsky, welcome to the Diet Doctor podcast, thanks so much for joining me.
So, I went to medical school with that thinking. I wasn't sure if I was going to do endocrinology or some sort of preventive medicine or family or internal medicine, but eventually after medical school, I decided on family medicine. So, I went into training at VCU over in Virginia with a real focus on nutrition, exercise, and lifestyle medicine, with a good combination of pharmacology and everything like that to combine it, to really hone in on helping prevent/cure chronic disease.
So, I had to really look into nutrition and exercise science to build muscle, improve my performance to get good. So, then once I became a state champ, really thought this is cool, but then again, wanted to use that information, just to give a fraction of it to the general population because that's how you really prevent and cure chronic disease.
So, did you find it hard, like it was lacking as you were going through the schooling?
So, exercise has sort of been knocked down in terms of its place and lifestyle in some circles. Now, personally, I have a problem with that because I think it's important and I'm sure you do as well. So, give us your thoughts about that. Is it true you can't outrun a bad diet? What is the place of exercise in health and weight loss in your mind?
But if you have just a little bit of nutrition going for you, the exercise can very much optimize your body composition and weight loss efforts. Most importantly though, the energy gap after you lose weight using nutrition... really bringing your physical activity back, we're starting to see a lot of the data that show that those who keep the weight off are the ones who are most physically active because of that energy gap difference.
So, ideally, a combination of all of it. You're not going to be able to recover every day if you're doing high intensity interval training and lifting. So, ideally, you'd have some steady state in there to help with recovery. It could be very good for endothelial function and everything like that and just being able to recover while burning more calories as well, just from a weight loss standpoint.
But then as I started getting more into the path of physiology and you start becoming insulin resistant and lipolytic because the insulin is not even working, etc, etc. and then having some of these patients that were losing weight on a high carbohydrate, low-fat, vegan type of diet. And it was like, okay, maybe there's more to it getting more into the science. I became good friends with Kevin Hall, you probably know who he is. And a lot of these other scientists.
And so, the way I view it is that the hormonal hypothesis is... those are very important because those can tell you where you store your energy, and also not only that but maybe changes in appetite and inflammation and things like that.
So, it's very important and it goes along with the calories in, calories out energy balance hypothesis, so... I kind of view them as together and you can't separate them, because obviously you can't give somebody 100% fruit juice... yeah, sure if they drink 800 calories of apple juice a day, they're going to lose weight, but how are they going to maintain that? They're going to feel miserable type of thing, so that's where my stance is right now.
And I don't know that we have great data to support that, you know. When you compare low-carb versus low fat diets for weight loss, the low-carb diets uniformly work better at six months and 12 months and a lot of the studies, the curves kind converge and compliance goes down. And it makes it really hard to know scientifically what the right answer is.
A cookie crisp but it's a children's cereal. It has whole grains, 10 g of whole grains per serving and it's like... I wouldn't give my daughter this cookie crisp cereal for breakfast every single day. It would be easier just to say, hey, go to a low-carb diet then get that completely out of your vision anyway. So, that's why I do think that a low-carb diet in this current environment is easier to stick to, that's what I think.
Whereas with the low-carb diet, you mentioned there is some insulin resistance there. But I think we need to sort of differentiate the insulin resistance with hyperinsulinemia, so the generalized insulin resistance versus the more localized insulin resistance like the muscle level with still lower insulin levels. So, do you differentiate in your patients with those and kind of look for that?
So, going to a lower carb diet tends to cut those things out anyway. They're usually not replacing those things with like lentils as I said. So, I tend to try to go for weight loss in general. I do use weight loss drugs if needed if I find that they've tried multiple times and that they haven't passed. So, I have my obesity certification everything like that, so I do use things like GLP1 agonists, you know.
If they've tried multiple times, for some reason their appetite and cravings, even on like ketogenic type of diets, but I do use those in general. I try to get them to cut calories, but they tend to be more of those hyperpalatable high carbohydrate foods.
So, yeah, I do tell them like a well-formulated ketogenic diet can be therapeutic in appetite regulations, similarly to these drugs that we use. So, if they're willing to do that, we definitely do that. Sometimes people just aren't willing to do it, and I especially like the Virta studies; if you can monitor them with the ketones, you can see that they're adhering. But a lot of the time patients are like, I'm not going to do that.
And lower fat, high carb is not going to work for everybody, but people want the sort of this black and white, just tell me what the diet to follow is that's going to work for me, where it's not always so clear cut. And there's not even necessarily a progression, I guess that's what I'm trying to get at, do you have a progression? Like try keto first, then try low-carb... but isn't a progression but-
And there ends up being a selection and survivorship type of bias because these companies are known for doing well with this particularly method, so when they see people doing well they hear that, "What's their method?", and they go, "Oh, I could probably do that", and then they get more success with that method. And then the same thing you see with the whole foods plant-based people, you know, they're all yelling at each other, this is how I lost 100 pounds, it's like that's how you lost 100 pounds.
Then you get a carnivore person who's lost massive amounts of weight, and obviously I can do this and the vegans, you know, are saying that's not possible, that's not good for you. And it's like that person lost 100, 200 pounds from what it was, and that's pretty good for them, and if they can stick to that, more power to them. That's kind of the way I am now. #It's a good approach to realize the way and there are lots of different ways out there. But also that weight loss is a new metric, that's so important. It's weight loss, it's how do you feel, insulin levels.
But it was then after the Improve-IT trial came out that it showed no, it actually did lower outcomes once they looked further past the surrogate marker of the CIMT. It actually did improve outcomes and this drug works in a different way than statins do, basically decreases the absorption of cholesterol in the intestine. And that's like okay, maybe there is something to this LDL hypothesis, and so I started going to the NLA meeting, Dr. Dayspring, if you know who he is.
But put into perspective though, it's one of those trials where they're going to say it was a 20% reduction, when in reality it was a less than 1% absolute risk reduction. So, less than 1% of the people saw benefit in reduction of heart attacks, but it was a benefit. And that's one of the dilemmas we fall into is seeing a benefit but seeing such a small benefit is okay, it's statistically significant, is it clinically significant for that one patient you're seeing and does it then confirm an entire model saying that LDL is the more important thing.
And these concepts don't have simple answers to them obviously. So, it's clear that LDL is involved but like you said, there's more to it than just LDL. So, part of the problem I have is controlling for metabolic health. Like all those studies, every LDL study has been done in a low fat or high carb or a standard American diet type of setting, and they don't generally control for metabolic health. So, now, what is your take on putting LDL into perspective with HDL, triglycerides, the ratios, the metabolic health? Do you think it has the same prognostic value with high HDL, low triglycerides and good metabolic health?
So, say for instance a smoker with hypertension... they'll have accelerated atherosclerosis with the same amount of LDL particles as you know, compared to someone who's very metabolically healthy. So, that area underneath the curve will be accelerated for atherosclerosis for those people with multiple other risk factors.
Now, you can look at somebody with familial hypercholesterolemia and that's- when you go into med school it's like yeah, those people don't have any other issues, it's just a genetic cause of their LDL receptors not working or their APOB is not connecting to their LDL receptor or whatever it is... they have a high area under the curve of LDL particles. But then when you dive in deeper, there might be more problems with people with FH and the scavenger receptors.
Lots of other things that can't necessarily extrapolate that data to someone who has a low-carb ketogenic induced- I actually have a... I'll add a document, I do want you to publish this blog for Dave Feldman because he's asked me to write, if I'm going to argue against someone who doesn't believe that the ketogenic induced LDL, if you want a hyper lean mass couple responder, if they're not a- what would you do to argue against that?
And I've listed out all the different arguments actually being in some of the Facebook groups, and a lot of the ketogenic proponents, they do have a lot of good arguments against the LDL hypothesis based on their hypothesis, so yeah. But I'll add you to that document because I think you'll appreciate it.
So it puts us in this realm of- we don't have the data to say it's safe, but we can also say that none of those people are represented in the LDL or statin trials, so where does that lead us? So, you can either say that we go back to the data we already have and say it's potentially harmful, or you say we've made some many improvements and all these other things are improving that we're going to continue to monitor.
So, if you were to recommend to somebody that they continue to be monitored with an elevated LDL on a low-carb diet with all the other health markers improving, what would you say, or how would you say they should be monitored moving forward?
Then, I talk about the risk, and I go, we don't have the data, but you've improved all these other risk factors, you're feeling so much better. We talked about quality of life... If you're feeling miserable on multiple medicines and you have a lot of excess weight versus you're on a ketogenic diet, you feel amazing, you've lost this excess weight. Who am I to say then, you know, this isn't good for you?
We don't have the data, so I'm talking to them like I'd be talking to you, like another physician or scientist that's looking into this. And I lay it out for them and they have autonomy. Other doctors I have seen... these low-carb groups, the doctors fire their patients because I think they don't want to get sued.
I am not exactly sure, but I tell the patients, I go, "Look, I think there may be an increased risk, but I don't know, if you feel better you have autonomy, you can choose this, you can choose to go on a statin or not, you can tell me, 'Off!' or you can just drink butter and not do any of the monounsaturated fat that I recommend." So I think patient autonomy is important but I lay it out for them.
There is so many paradoxes for the LDL hypothesis and it just tells you that it's not so cut and dried, and I guess that's my problem with the whole lipidology world. They do sort of paint it as a little bit too black and white from my standpoint, and I can understand why, but do you see that too? Do you think it's a little too black and white?
And it's just... I am baffled because I didn't even think you could have some of these exponential increases in LDL. I mean I saw it in practice, but not to levels where people would have homozygous familial hypercholesterolemia. And that's where you would have two knockouts of various parts of the genes having to do with LDL receptors and APoB.
Spencer: 400, 500, 600. And so I'm seeing this in the group, and I'm like no way, it's got to be something else. But then you see their LDLs before they went on a ketogenic diet and they are like 130s, 140s, 150s. And so, I'm actually writing... I'm going to publish a case series on about five of these individuals. I actually brought it because I'm going to UCSD next year and the reason I am going to UCSD next year for preventative medicine is to get a Master's in public health, get some more bio stats, and also to get some more mentorship to put this study into fruition, make it come to life.
And basically, I'm going to publish this case series because people don't believe it. I've actually talked to multiple doctors out there, I've sent the lipid profiles of some of these patients and they think no way, they have to have thyroid, they have to have type 3, whatever, they have all sorts of things, and I'm like no, it is ketogenic diet induced.
We can't find anything. I can't see anything with the snips, there is no LDL receptor issues, their urines are fine, you know, they don't have nephrotic syndrome or something like that, their thyroid is fine, they don't have a family history of hyperlipidemia, they do not have anybody with coronary disease in their family, they're lean, no other medical problems, ketogenic diet, you know. 400, 500 LDL mg/dL.
So what we want to do is we want to basically get like 50 of these lean mass hyper responders and then we would really want to get a control group of low-carbers who don't have this massive increase, with similar metabolic profiles and then just watch progression. Now as we talked before, probably we will never going to have the hard outcomes we're looking for but at least progression in atherosclerosis. And I'd like to look at the lumen with like a CT angiography. I don't think a CAC score would do it, I think too many people... If they are young, you're not going to see that calcification.
And it's not just like a 20, 30 ml/dL increase that you see with some of these individuals, we're talking massive increases; 100, 200 ml/dL. We should see an effect... similar timeframe, area under the curve, APoB, LDL particles that you would see with someone with familial hypercholesterolemia.
Yeah, they've had it since youth, but you should see in a similar timeframe that progression. If we don't see that massive progressions or any progression or any difference you know, maybe there is something else going on there, that's protective. Just the study that came out is talking about scavenger receptors and how we thought that the LDL particles moved passively- you know, depending on their size in the endothelium. Just this new study showing that maybe they had to go through their scavenger receptors, you know.
Maybe there's something protective about the ketogenic diet that down-regulates this process. And I just think it's fascinating because I just want to look... Dave and I talk about it. It's a win-win situation... I just want to see... maybe this would be a breakthrough, and if it does show massive progression as I would predict, then you know, that's the data we need to know.
It's... don't be so ideological, but really search for the data, understand the data and understand what we don't know and what we need to know and help us get there. And we talked a little bit- I guess this segues a bit into people... who they are in person and who they are on Twitter and it's humorous because people can be such jerks on Twitter and it sort of makes you lose sight that what we're really doing is trying to help people improve their health. So why do you think that is? That people just become so just snarky on Twitter?
But in general when you're behind a computer you don't have that personal connection, like can you imagine me saying certain things right here to your face are here that are just like all my gosh... that some of the people say on Twitter... Like swearing, almost threatening in certain ways.
I think if we step back so take for instance, I don't know, vegans or whole foods plant-based individual proponents and then the people on the other end to be like the carnivores like Dr. Baker and how a lot of people is yelling at each other and kind of making fun of each other and I don't mind teasing each other in good fun but I think when you step back and go to someone like Disneyland and Walmart and see there's a lot of people... they'll never follow a whole foods plant-based or a carnivore. I've tried to prescribe a carnivore diet as much as I like-
Personally I don't think it's probably optimal but I've actually prescribed it to patients who I thought it would fit and they just wouldn't stick to it, which is interesting. So if you take a step back most people are just eating just absolute horribly. If we can even get them closer aligned to any type of these diets, ketogenic, low-carb high-fat, whatever you want to call it or a vegan-esque type of diet, I think we have proven most people just have no awareness.
And so I think if we all kind of- We're all trying to help people. I do think more people need to come across the party lines or whatever, go to each other's conferences, understand where you're coming from and I do think, you know, there's industry involvement that's kind of pushed us maybe one way or the other and there is influence there and I would be naïve to say, no, it has nothing to do with it.
I think we do need to be skeptical about a lot of things and I think we all should just come together and realize we just try to help people.
Lots of vegetables, lean protein, a little bit of healthy starch, healthy fat thrown in there. That is kind the way I do it. Eight hours of sleep... very standard kind of boring stuff, but like the stuff that we know is good for you. Very, very simple.
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