Nick Norwitz
speaker
450 appearances
2 recordings
2 series
first heard Apr 2025
last heard Apr 2025
Nick Norwitz’s voice in public audio — every appearance, attributed to the second.
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Appearances
And I think the challenge I want to present your listeners with is really grapple with the ideas and the words I'm saying and hear how these ideas are actually consistent, not conflicting, and how context is really important. Let me first actually attack that idea of LVL and Applebee being causative in heart disease, because indeed they are. And by that, I mean they're part of the causal cascade.
So if you didn't have ApoB or LDL particles or they were at the floor, you really can't develop heart disease progression. That's true. But it's also true that context, metabolic context really matters. If two different people have the same exposure to LDL or ApoB. So the same level, how high it is for the same duration of time. Will those two people develop heart disease at the same rate?
And the answer is no. There are other factors that influence what the absolute risk or absolute progression rate is. Some person might have really rapid progression. Other person might have such minimal progression that it's basically negligible. You can think about it as kind of if you like, you're mathematically inclined, a little graph.
And on the x-axis is exposure to LDL, exposure to LDL, cholesterol exposure to aqua B. And the y-axis is how much plaque actually accumulates in your heart. Some person can have a very steep slope, meaning with a little exposure, they get a lot of plaque.
And other person could have a very shallow slope, meaning for a ton of exposure, they actually develop very little or maybe even no plaque, not even a measurable amount. That difference is really, really important because people are trying to decide what to do with lifestyle or whether or not to take medications that do have side effects.
And in the context of a whole person, you always have to do this benefit analysis. It's not about snapping your fingers. You can't snap your fingers and change one biomarker in isolation. Say you're using a ketogenic diet to treat inflammatory bowel disease, but your LDL is really high.
Well, it's important to know what's the absolute risk because what you might be trading by reintroducing carbs is an increased risk of flares and ending up in the hospital or trying a medication that might have side effects, promote insulin resistance or other negative health effects that you don't otherwise want. So I'm not here to say that LZL or Applebee is irrelevant.
I'm here to say it's context dependent and that in assessing an individual's risk, you need to take a look at the whole picture. So, you know, TLDR is going over your head. Don't get your medical information, your health recommendations off of podcasts and YouTube. I'm here to provide information. But at the end of the day, key thing is to assess your own risk profile.
But with that caveat in place. A question that I think we should ask is why does LDL go up? We talk all the time about LDL, but not so much about the physiology behind what drives it. And people then tend to oversimplify and think, oh, it's just saturated fat. They're just, quote, butter guzzlers. Or it's just some quirk of genetics, right? Those are kind of hand wavy statements.
And in some cases, they're true. Saturated fat can increase LDL, at least a little bit. Genetics can play a role. But when you have a really interesting phenomenon, like someone going low carbon, their LDL going for like 300, 400, 500, saturated fat almost certainly isn't the only thing at play. And in some people, it's very weird because they even go like plant-based low carbon.
They'll still see this response. I can actually get to my LDL for like 300, 400 on a vegan keto diet. So you get to ask the question, well, what's going on here and what can we learn from it? That's where this population that we've been studying comes into play.
Because what appears to happen when lean insulin sensitive people go low carb is when they're no longer relying on carbs as much for fuel, specifically what happens is the carb stores in the liver, which defend blood glucose stores when they drop, it triggers this cycle whereby you're burning fat
And some of the fat that kind of, you could say, spills over gets taken back up into the liver and then recycled through the body through a trafficking system that depends on cholesterol. So specifically, you have these big, you could say, fat-carrying boats. They're called VLDL particles, very low-density lipid particles.
You need them because fat, stored fat, doesn't mix with aqueous solution, so water. You know that if you take water, Oil, you put it in water, it doesn't mix. So it's the same way with fat in your body. It doesn't really mix well with blood. So you need a way to carry it around the body. And it gets packaged, the fat, into these shipment containers that contain cholesterol.
And in circulating around the body and dropping off fat back at fat tissue and muscle tissue, the result of that can be very, very high LDL, which can actually be reversed in these people by just adding back carbs, which is why I can lower my cholesterol with Oreo cookies, which I've done and published on. You're laughing now, and it seems like a joke, and to some extent it is.
You have to ask questions like, well, why would I do a stunt where I publish a study where I lower my cholesterol with Oreo cookies? It's not because I think Oreo cookies are a health food or I want people to eat them, but I want to get attention to this fascinating physiology. Yeah, of course. It's clickbait for me to eat Oreo cookies and lower my cholesterol. It's also legitimate science.
And if it opens up a conversation about what's going on here, what can we learn about this population, and how can we rally to study this population, I think that's very worthwhile. I just want to make the point that in science, the greatest discoveries, let's say the most impactful discoveries, come out of just pursuing these curiosities. Why does my cholesterol go down when I eat Oreo cookies?
Why does Gila monster venom screw up the metabolism of its prey? People studying Gila monster venom in the 90s, they didn't know what would happen as a result of the studies. Guess what? The result of the studies is basically the modern era of weight loss drugs. Ozempic, Wigovi, GLP-1 receptor agonists are a result of studying Gila monster venom.
In the same vein, what we're doing now can have knock-on effects and knock-on discoveries that I think are generalizable to every single human being. If just then now in the modern era with social media, people get to see it happening, the science happening in real time.
What I would say is, why do they have a baseline? Well, these people, the average age at time of enrollment was about 55 years old. And at that point in time, average time on a keto diet was 4.7 years. So if you do the math, these people didn't start a ketogenic diet on average until they were over 50. So they had the first 50 years of their life when they were doing other things.
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