Transcription
I read through the keto CTA preprint. Yeah. So they have a new paper that's come out. I'm not sure if you've seen it. Their first one was retracted. Yeah. And then they've done a second paper where they used different analyses from different AI software, HeartFlow, and then another company called QAngio. Right, same data set looking at 12 months apart, these people on a keto diet, what's happening in their arteries.
First thing I'll say is to my knowledge, even HeartFlow, there's very little validation against IVUS in subjects with subclinical atherosclerosis. Correct. That's an important thing just to state. Insignificant. Because how accurate is it in this population where there's only a very small amount of plaque at actually detecting it and reporting accurately when there could be a lot of noise. And I believe there's no validation looking at validating it against IVUS across two different time points and looking at progression. That that body of evidence doesn't seem to exist.
In that preprint though, I think it's important for people to understand that using HeartFlow, 65% of subjects had progression. Using QAngio, 85% of subjects had progression. So there was a little bit of discrepancy between the two, but there was progression. And about in QAngio, about 20% of people had rapid progression. And HeartFlow said zero. But across the board, there was agreement that most people were getting some progression. And then the question is, you know, what is that progression compared to a control? There's no control group. Right. So it's very hard to to answer that.
All I'll say is I did HeartFlow, which is what they've done. And I did it 16 months ago. And I repeated it last month. And how are your arteries? And this is why I wanted to understand what the evidence base is for validation because I also want to understand when I get my results as an individual, what do they mean? Right. And my apoB sits at about 75 through through diet. I guess I'm I'm lucky that my genes respond pretty well to dietary change. Usually I sit about 120, 130 when I'm eating you know, when I was before I was 30 years old, before I changed my diet, eating a lot of lamb and beef in [snorts] in Australia and stuff. Yeah. So So my apoB and LDL went down from that 120 to 130 down to 70s. Good. And I'll say from Heart Flow and I I've got an episode on this, I had uh total plaque regression 48% over a 16-month period. Awesome. Now, the question is what does that mean? We don't know. How reliable is that? How accurate? I'm not going to read into that too much. Yeah. I'm happy that it suggests I don't have rapid progression, probably. Um, which is great. But I'm not going to use that as a rationale to not lower my apoB down a bit more because of all of the other evidence that shows when apoB is down, you know, into 40s to 50s, based on the studies I've seen and the advice I'm getting, that's where you see much more regression and stabilization of plaque.
Stabilization of plaque is a mildly controversial item. We do see plaque thickness of the cap. It's not necessarily consistent across all studies, but it's enough evidence there that we say it appears that the plaques are stabilized, they're calcified, and they seem to appear to be stabilized. And the data sort of bears that out over time. And the PCSK9 data now shows regression of plaque pretty reasonably at lower levels.
When you say lower level, like sub sub-50? In the 40s and below. So, that yours responded and lowered makes me wonder how did that happen cuz you wouldn't think by the current models that it should lower from 120 down to 75. My LDL? Yeah. You would think that that shouldn't you shouldn't see a regression of the plaque there. You wouldn't see a regression of plaque from at at 70 mg/dL is what you're saying? Yeah, generally you don't see that in other studies. But, you're also dealing with plaque numbers on you that are probably so minor and that it's really hard to make sense of what that is and might be in within the statistical error. So, the question is what would you go on? Now, if it were up to me, I would go on a PCSK9 inhibitor because that seems to have a lot of benefit or
Why would you if it So, for me it looks like monotherapy will get me to below 50. Ezetimibe will be all you need. My guess is if you take Zetia, you'll be fine. So, that was actually something that I proposed as a question to Dan Soffer who's going to come back on the show. He he he didn't disagree with that, but he also said, "Look, there's so much outcome evidence for statins and what what if some of the benefit of statins is not driven by LDL that statins also have a mild vascular anti-inflammatory effect. Now, before I did bariatric surgery, I used to do vascular surgery. And it was very very clear that we would see people coming in with problems with their peripheral arteries when they had stopped statins a couple weeks before we would get these emergency black legs. You know, I'd be fishing out clot and stuff. And so, we've known for a long time that statins have this mildly anti-inflammatory arterial effect, whatever that means. So, yeah, it's not And if you can tolerate the statins without a problem and I have no problem with mine, you may or may not have a problem with yours. It's not a bad thing.
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