Nick Norwitz

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.

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.

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.

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.

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?

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?

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.

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.

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.

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.

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.

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.

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