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
uh all put out no and make anxious sperm so don't do it i know it's uh yeah anxious sperm is it worth it to you to risk a potential impact on the mental health of your future children which you'll never know for sure say they develop anxiety you'll never know if it was your fault or not you will never know but is it worth it to you to have those two diet cokes per day is it yeah and i would say it's just like for me no if if it really matters to you that much
If you're an individual, you can make an adult decision. If you're a kid, it's not mine.
I love that. My karate sensei and I got matching stay curious tattoos. I love that.
We had a bunch of other things we were going to talk about. We decided we actually found out this morning our paper got accepted. So we're kind of pivoting. You had a lot of enthusiasm in that opening. I hope I can deliver. But this is truly an exciting moment with this paper getting accepted because it is a first of its kind study.
It's been one that my colleagues and I, Dave Feldman and Adrian Sotomayor, have been expending blood, sweat and tears on for a few years. And I really have to give most of the credit to Dave Feldman. This started with him. He's, if you don't know him, an outsider, an engineer who had this provocative question. We'll get into it.
Delved into lipidology, became obsessed with it, crowdfunded a clinical trial and executed on it. And we've been working on this area of research. We've had like 10 papers on it over the past couple of years.
But this is really the landmark study because what we did, what the team did was take this group of people that turned lean mass hyper responders, these people who go low carb and see their LDL go through the roof, like sky high levels and followed them
over the course of one year with high resolution CT angiography to look not just for calcified plaques, but also non calcified plaque to see does plaque progress in this population that conventional wisdom would say is that super, super high risk their LDL levels are 200, 300, 400, 500. Sometimes it's close to 600. We had one person in this trial with an LDL of 591.
So do they have plaque progression like conventional wisdom would predict? And if there is plaque progression at a population level, what actually is the major risk factor? What drives the progression? And I'll just give you the headline. There was no or minimal progression in the majority of people.
On a population level, there was a tiny bit of progression, something called percent atheroma volume increased by 0.8%, which is pretty modest at a population scale. And the really critical thing is in addition to most people having no or minimal progression, you had to ask what predicts progression? Is it this LDL cholesterol that we always hear about or the associated marker ApoB?
And the answer was no. Actually, there was no predictive value, no association between ApoB and plaque regression or between LDL and plaque progression. LDL and ApoB did not predict plaque progression. What predicted plaque progression was whether or not somebody had plaque at baselines. So you can get functional tests of your heart.
These are becoming more and more mainstream to help people individualize their risk and their treatment decisions. Something called the coronary artery calcium scan is one. And the CAC score, this functional test looking at the heart, did actually predict progression. So basically, if you had plaque to start with, you were more likely to have that plaque progress.
If you didn't have plaque to start with, then you were unlikely to have progression. And LDL and Applebee were pretty much irrelevant in determining or predicting whether or not plaque would progress. which is really astonishing given the levels of LDL in this population. Again, 200, 300, 400, 500 LDL. It's quite remarkable.
And I just want to emphasize one more thing, and then I'll get off my monologue. The really interesting thing about this population, lean mass hypersponders, is they are the first and only human population we have ever studied that has high LDL as an isolated variable, a
apart from metabolic dysfunction, because a lot of people are metabolically unhealthy in the population, and that changes the metabolic context, and apart from genetic drivers like familial hypercholesterolemia. So it's true if you have a broken lip metabolism. There are some people that are unlucky enough to be born with this.
If you have a broken lip metabolism, you can have very high LZL and also typically have advanced heart disease at an early age. Something called homozygous familial hypercholesterolemia. Kids will get heart attacks at like, you know, age... This is different because it's not that these people have broken liver metabolisms.
It's that in cutting out carbs, sometimes even irrespective of saturated fat intake, in cutting out carbs, there appears to be a metabolic response whereby the cholesterol trafficking, fat trafficking system gets upregulated. And as a result, an epiphenomenon, you could say the LDL goes through the roof.
So this is really a complex story that I'd love to get into with you about novel corners of physiology. resulting in pretty dramatic cholesterol lipid profiles that give most cardiologists heart attack by proxy. By that, I mean it's very shocking. And then examining, well, what's the mechanism behind this? And also, what does it mean for risk?
And these new data say the risk profile might not be what we would otherwise think if we weren't studying this population.
Right. So I think we're going to have to step back and go through some of the framing literature, but also make the critical point that some of the things you said that might sound at odds with what I said, like Apple being LDL being causative, are actually consistent with what I said.
Showing 221–240 of 450 · page 12 of 23
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