Nick Norwitz

So if you look at large-scale population studies, like having type 2 diabetes, prediabetes, high insulin resistance score, like an LPIR or a HOMIR, is a very strong predictor for poor cardiovascular health.

So I think you can kind of cluster into two possibilities. One is that there are just underlying susceptibility factors that we didn't identify in this study. So the people with plaque at baseline are probably, let's say there are like genetic factors that make one more susceptible to heart disease.

So I think you can kind of cluster into two possibilities. One is that there are just underlying susceptibility factors that we didn't identify in this study. So the people with plaque at baseline are probably, let's say there are like genetic factors that make one more susceptible to heart disease.

So I think you can kind of cluster into two possibilities. One is that there are just underlying susceptibility factors that we didn't identify in this study. So the people with plaque at baseline are probably, let's say there are like genetic factors that make one more susceptible to heart disease.

Even irrespective of LDL, ApoB, there are other factors that genetically could predispose somebody to heart disease. The people that have plaque at baseline are more likely to have those factors. So it could just be these are the folks that have other risk factors for heart disease, you know, in their genetic code, in their microbiome, in their epigenetics, whatever.

Even irrespective of LDL, ApoB, there are other factors that genetically could predispose somebody to heart disease. The people that have plaque at baseline are more likely to have those factors. So it could just be these are the folks that have other risk factors for heart disease, you know, in their genetic code, in their microbiome, in their epigenetics, whatever.

Even irrespective of LDL, ApoB, there are other factors that genetically could predispose somebody to heart disease. The people that have plaque at baseline are more likely to have those factors. So it could just be these are the folks that have other risk factors for heart disease, you know, in their genetic code, in their microbiome, in their epigenetics, whatever.

The other possibility, which I think is more interesting, is that the plaque itself, which is kind of like an inflammatory microenvironment, could propagate, self-propagate, that plaque gets plaque, that the inflammation there locally, the activated immune cells could perpetuate more plaque growth.

The other possibility, which I think is more interesting, is that the plaque itself, which is kind of like an inflammatory microenvironment, could propagate, self-propagate, that plaque gets plaque, that the inflammation there locally, the activated immune cells could perpetuate more plaque growth.

The other possibility, which I think is more interesting, is that the plaque itself, which is kind of like an inflammatory microenvironment, could propagate, self-propagate, that plaque gets plaque, that the inflammation there locally, the activated immune cells could perpetuate more plaque growth.

So think of it as like if a seed was planted and you see the sproutling growing, it's going to keep growing. Right. Versus if the seed was never planted in the first place. You know, this study didn't answer those particular questions, but they're great questions to ask because they are the frontier of what we need to study next, because this is all about individual risk assessment.

So think of it as like if a seed was planted and you see the sproutling growing, it's going to keep growing. Right. Versus if the seed was never planted in the first place. You know, this study didn't answer those particular questions, but they're great questions to ask because they are the frontier of what we need to study next, because this is all about individual risk assessment.

So think of it as like if a seed was planted and you see the sproutling growing, it's going to keep growing. Right. Versus if the seed was never planted in the first place. You know, this study didn't answer those particular questions, but they're great questions to ask because they are the frontier of what we need to study next, because this is all about individual risk assessment.

And so, you know, trying to identify, like, why does person X have progression or person Y not? Partitioning those groups and then also looking at the outliers, like, that's where we learn so much. To double down on that point, you know, some people, they see someone with it.

And so, you know, trying to identify, like, why does person X have progression or person Y not? Partitioning those groups and then also looking at the outliers, like, that's where we learn so much. To double down on that point, you know, some people, they see someone with it.

And so, you know, trying to identify, like, why does person X have progression or person Y not? Partitioning those groups and then also looking at the outliers, like, that's where we learn so much. To double down on that point, you know, some people, they see someone with it.

We have one person, actually not even a person in the study, but a person that's in a movie related to some of the research we're doing. You know, they're, you know, I'm about to turn 60. Their LDL is around 700. And they have no plaque on coronary CT angiography, none that can be measured. That's remarkable. That's jaw dropping. And some people may say it's just an N equals one.

We have one person, actually not even a person in the study, but a person that's in a movie related to some of the research we're doing. You know, they're, you know, I'm about to turn 60. Their LDL is around 700. And they have no plaque on coronary CT angiography, none that can be measured. That's remarkable. That's jaw dropping. And some people may say it's just an N equals one.

We have one person, actually not even a person in the study, but a person that's in a movie related to some of the research we're doing. You know, they're, you know, I'm about to turn 60. Their LDL is around 700. And they have no plaque on coronary CT angiography, none that can be measured. That's remarkable. That's jaw dropping. And some people may say it's just an N equals one.

It's just an anecdote. You can say that if you want. I prefer to say this really rubs up against the status quo. Yes, at a population level, this person is an outlier. Don't you want to know why they're an outlier? Don't you want to know what makes them resistant? Because once you figure that out, that's the seed of a solution that could generalize to more people. So I love studying the outliers.