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Oct 08

Guesting on the Peter Attia Drive (2 of 5) – Cholesterol Challenge, Lipid Metabolism, LDL Receptor

 

This is a five part series covering my appearance on The Peter Attia Drive podcast. Please skip to the final post to comment. 

Part 1 of 5 – Lean Mass Hyper-responders, Oxidized LDL, All-Cause Mortality
Part 2 of 5 – Cholesterol Challenge, Lipid Metabolism, LDL Receptor
Part 3 of 5 – Remnant Cholesterol, Craig Moffitt, Fasting
Part 4 of 5 – Energy Status, Risk, Testing the Hypothesis
Part 5 of 5 – Comments and Featured Thoughts

 

The Low Carb Cholesterol Challenge

Dave Feldman

The part of what this energy model, in particular, that with hyper-responders, specifically lean mass app responders comes back to. I don’t know if you’ve, I know you don’t necessarily hang out on Twitter too much, but you know that I’ve had-

Peter Attia

More than I would like.

Dave Feldman

I have this pinned Tweet, I’ve been pinging lots of lipid-lowering experts on this, I’ve said, “Look, I’m looking for any studies that show people with high LDL will have high cardiovascular disease, if they likewise have high HDL and low triglycerides.” But there’s one qualification, it can’t be a gene or drug study. It’s gotta just be-

<Snip>

https://twitter.com/DaveKeto/status/963437664199352322

Peter Attia

No, I’m seeing that. Here’s my concern with that, Dave. I have no doubt in my mind that you are a truth seeker. I don’t think that’s true of necessarily some of your peers. I do think a number of your peers are deluded and so filled with their own confirmation bias, and so unwilling to acknowledge that their precious low carbohydrate diets could be hurting them. That not with malicious intent, but with blind carelessness, they are absolutely ambivalent to anything.

I don’t put you in that category, so I will challenge you in the following way…

Dave Feldman

Great.

Peter Attia

When you say, “Show me an example of something that is not a genetic study, that can point to that phenotype.” The reason I would call issue with that is, why would you limit yourself from genetic studies? That’s sort of like me saying, “I want to know if there are people who are six feet tall. I think they might be, but I’ve never seen one. So, if you can go into a kindergarten class and find me one, I’ll believe it. But, you must limit yourself to the kindergarten class.” In other words, that’s an obscure example. What I’m basically saying is, you’re excluding so much potential data by excluding all of the genetics.

Because when people talk about genetic studies, we have to remember something, most of the genes, most of the snips that lead to alterations in lipids and lipid metabolism, are completely unidentified. FH, for example, familial hypercholesterolemia, which would be the most obviously example to counter that point, you’re excluding because it’s a genetic condition. What the listener might not know is that FH is a phenotypic diagnosis, not a genotypic diagnosis. FH is arguably the most heterogenous collection of genes you can imagine.

So, why would we exclude looking at those people, when that’s, in many ways, one of the richest bodies of evidence for a natural experiment in … To answer the question, can you have LDLC, high HDLC, low triglyceride, and still get atherosclerosis? That’s the question you’re asking, right?

Lipid Malabsorption – Part I

Dave Feldman

Yes, yes. Well, so, we’ll double back to that in a sec, but basically, you’re taking us back to genes, and this is why … This is another hypothesis, fully untested, I’m in the process of trying to collect on it, but I call this loosely, Cellular Lipid Malabsorption. Right, just generally shorten it to lipid malabsorption.

Basically, here’s the issue that I have with the existing mendelian randomizations. For that matter, almost all of the gene-based studies is what we’re trying to get, what we’re trying to get, is as much as we can, the isolation of just a higher gradient of LDL particle count. That’s what we all secretly … We want your wand. You’re talking about where we can wave it, and then there’s just magically more LDL particles in some people, or for that matter, less LDL particles. Without touching any other parts of the process.

The problem is, that I believe … I’m keeping a list of my own SNPs of those genes that are either resulting in higher or lower LDLC. Unfortunately, of the ones that I find in the mendelian randomizations, they don’t just result in the higher LDLC and LDLP, they also come to be that way because there’s a lack of lipids or lipoprotein uptake by the cells.

Therefore, particularly with endothelial cells, you’ve got to be concerned that that could cause dysfunction. And therefore could be a reason for why you’d have higher levels of atherosclerosis. This is why-

Peter Attia

Wait, wait. So, explain that part again. The last part.

Dave Feldman

We would ideally want to-

Peter Attia

No, no, I got that part, but tell me about what you said about the endothelial cells?

Dave Feldman

Endothelial cells being dysfunctional.

Peter Attia

Yes.

Dave Feldman

Would that be potentially problematic for atherosclerosis?

Peter Attia

Yes.

Dave Feldman

Okay, then why would we want to look at any SNP that would in any way impair, inhibit them relative to a normal person endothelial cell?

Peter Attia

Why do we believe patients, or a subset of patients with FH, as a result of their FH have defective endothelial cells?

Dave Feldman

Well, if you’ve got defective LDL receptors.

Peter Attia

There’s not receptors on the endothelial cell. It’s diffusion mediated.

Okay — time out!

Endothelial Cells and LDL Receptors

This was probably the most surreal moment to me in the podcast as I found myself instantly conflicted.

I assumed going into the broadcast that we’d likely agree on all the fundamentals, yet would disagree on the broader interpretations. And should Peter correct me anywhere on a question of fundamentals, he was almost certainly right and I’d be all too happy to concede this on the spot (hence my “stealth interviewer” statement earlier).

Yet… Peter said something that I was 90% certain was in error. Endothelial cells do have LDL receptors… right? Peter said this with such specificity and confidence. Could I be wrong about this? I was suddenly searching everywhere in my head where I learned about endothelial cells and LDLr.

Regardless, the bigger problem is that endothelial cells were just one part of the larger equation to this central point anyway. If I got hung up on this point with endothelial cells, right or wrong, I might also fail to illustrate the larger one. The issue of Lipid Malabsorption was relevant to all tissues, so why not just move the spotlight to the other tissues and fact-check the endothelial cell receptor issue later?

Dave Feldman

Okay. Well, yes, but you’ve got the receptors with the Adipocytes, right?

Peter Attia

Yes, but, at least 20, if not 40% of LDL uptake, is not even receptor bound in the body.

Annoyingly, it was in this moment I remembered where I had first heard about endothelial cells and their family of receptors (including LDLr). But I didn’t want to doubleback as the moment as I really didn’t want to say anything on it until I was 100% sure.

Fast forward two hours…

After the podcast was completed and I got back to my car, I enthusiastically pulled up every reference I could on endothelial cells and LDL receptors. I further had Siobhan redundantly do the same. It all checked out.

Fast forward three weeks later to August 16…

I was at another conference in a lengthy tweet exchange with Nick Hiebert between sessions where at one point I said the following:

https://twitter.com/DaveKeto/status/1030113916540669953

To my surprise, Peter jumped into the debate (something he rarely does on Twitter) with the following:

https://twitter.com/PeterAttiaMD/status/1030124638909673472

Of course, now I was much more confident in the original assertion. But I wanted to keep this lighthearted and friendly so that my answer wouldn’t seem confrontational or curt in any way. So given many were pinging each of us about when the podcast would be released, I decided to insert a joke about that along with the pathway answer…

Peter then ultimately acknowledged this but expressed his reservations that evidence was thin for in vivo studies in particular (even if demonstrated in vitro). We then exchanged a few more tweets back and forth from there before stopping for the day.

Lipid Malabsorption – Part II

We now return the discussion already in progress…

Peter Attia

And not all cases of FH have receptor deficiencies. So, there are at least 2,000 vaguely identified genetic causes of familial hypercholesterolemia. Some of them are lower, they have fewer receptors. So, the PCSK9s are a subset of FH, right? About three to 5% of patients with FH have-

Dave Feldman

Over expression of PCSK9.

Peter Attia

Over expression of PCSK9.

Dave Feldman

Gotcha.

Peter Attia

But that’s how PCSK9 was discovered.

Dave Feldman

Okay, but in that case, you’re impacting a cell’s capability of uptake for lipids, or for lipoproteins, right?

Peter Attia

Yes, you are in that situation. Those patients’ livers, will take up less LDL, because PCSK9 is a protein that does, among other things, degrades the LDL receptors because they have hyper-functioning PCSK9, they are more rapidly degrading their LDL receptors on the livers, so they’re taking up less LDL particles. Which explains why they have higher LDL.

Dave Feldman

But this, again, introduces a dysfunction on the lipid metabolism itself.

Peter Attia

But that has nothing to do with the endothelial. That has nothing to do where atherosclerosis occurs. All that’s doing is giving you more LDL and circulation.

Dave Feldman

But, it’s … Let me put it this way. Why not take anything that results in a higher level of LDLC or LDLP that doesn’t impact any lipid absorption from any tissue at all?

Peter Attia

Right. But that might be a bit of an artificial constraint right? As you pointed out yourself and I think anybody listening to this will appreciate, this is a complicated dynamic system, so it is going to be difficult to have some perturbation in a system that will lower or raise LDL that won’t have some other effect.

The question is, how do we, with some reasonable degree of certainty, look at those other effects, and ask whether or not their germane to the question of atherosclerosis and the causality of LDL to atherosclerosis. So, I think the PCSK9 example is not an unreasonable one, because we have a pretty clear understanding of what that gene does. We have a very clear understanding of where that protein lives, and what it’s doing-

Dave Feldman

But if anything, that’s resulting in the other direction. Where, if you have lower LDLC or LDLP from under expression PCSK9. That actually results in a hyper-absorption of lipids, for example.

Peter Attia

In the liver, yeah. They have enhanced hepatic clearance. So both ends of that though, right? So, if you have hyper-functioning and hypo-functioning PCSK9 patients out there, both of whom exist, I believe the hyper-functionings were discovered first. But they hypo-functionings are kind of the ones that gave the drug companies the desire to go in … Not the desire, the idea to go and create a drug to mimic that phenotype. But these patients walk around with LDL cholesterol of 10 to 20 milligrams per deciliter, and as far as anybody can tell, there’s no other side effect of that.

Dave Feldman

This is the thing I want to zero in on. Let’s say that we do that. Let’s that we go “Okay, never mind this side part of the lipid hypothesis end of it. I’m sorry, the lipid metabolism end of it.” We should then be able to look back at these people with the more novel versions of SNPs and assuming there’s at least a large enough population, we should see that longevity. Your mentioning of the APOC-III from earlier, is the first that I’ve been able to find of that one. I’m interested to see if we would see that across the board with these people who have these SNPs.

Peter Attia

Yeah. I mean, I suspect it will have to do with how many of them there are, and how long they’re being tracked.

Dave Feldman

Because, the all-cause mortality, you’d have to understand, I sympathize with your concern, as it’s absolutely the case, nutrition medicine, there’s certainly a lot of personalities that are out there. But, I can understand at least for me, on my end, I like hard endpoints over soft endpoints. Maybe it’s just the engineer in me. I like ones and zeros. Death is pretty easy to diagnose. Whereas, soft endpoints, the downside is there can be arbitrary decision making on the part of the patient and the doctor.

Peter Attia

Yeah, you know, I heard you mention that on one of the podcasts. I gotta tell you. I disagree with that. Having seen more patients in an E.R. when I was in residency with MIs, I can honestly tell you, Dave, never once knew what their cholesterol levels were.

When someone comes in the E.R. with chest pain, I care about the advanced cardiac life support algorithm, which involves oxygen, which involves and EKG, which involves troponin, which involves morphine, aspirin, and potentially a trip to the cath lab. But, we are, and no where in that algorithm, are we asking, “What’s their LDL?” And letting that help us think, is this indigestion versus other things. So, I do take issue with calling MI as soft outcome.

There’s a little bit of a misunderstanding here. The podcast Peter referred to is likely my appearance on ZDoggMD. I have it queued to the specific part here:

To summarize:

  • Person A has high cholesterol and is told regularly by their doctor of this concern.
  • Person B has low cholesterol and is likewise aware of this through their doctor.
  • Each eats the same meal, experiences an intense 30-minute chest pain right afterward.

While I think each have a decent chance of checking themselves into the hospital, I certainly think Person B is more likely to rule it heartburn and take a tums. Person A checks in, gets an EKG, post-cardiac enzymes, etc. So if both A and B are in a study, we can see how their own cholesterol awareness furthered a feedback loop that could potentially bias the data. The only way to guard against this would be for both the doctor and patient to be unaware of the lipid numbers. (File that under Things That Will Never Happen)

Peter was speaking more to the admittance upon entering the hospital, not your primary care physician discussions. But as an aside, I think I could go into any hospital waiting room in America and over half the people there will know off hand if their cholesterol is “high” or not, regardless of why they are there.

Soft vs Hard Endpoints

Peter Attia

It’s not so much whether it’s a soft outcome. It’s whether or not there are things like, say revascularization. That can be determined based on the decision on the part of the doctor and the patient, that may or may not have to do with their knowledge of the lipids, right?

Agree. These are different things. But, I also think we should be careful not to take mortality as the only outcome. I will say this, and I hate putting on the stupid doctor hat, because it sounds ridiculous in this context, but unfortunately, I feel like I have to go back into and out of that world here. I would say at least half the patients that come to me, do not actually find themselves asking for an extension in life span. Right? My interest is longevity. But longevity has two components. How do you increase lifespan? Meaning, how do you delay death? And how do you improve health span? I won’t go into what that means, but, the bottom line is, there are many people who say, “I honestly have no interest in living one day long then I might otherwise live. But I want that quality to be much higher.” So, if we’re going to say … And, again, I don’t necessarily agree with that, I think the bigger issue is a statistical one with all- cause mortality, but, nevertheless-

Dave Feldman

But you go into modality. Like, if somebody has an MI, and it actually impacts their quality of life afterwards.

Peter talks a bit about possible modality outcomes, statin impact on Alzheimer’s and diabetes, and population vs individual-level data.

Dave Feldman

But, getting back to the challenge. In a sense, you’re saying by ignoring the genetic data, that the genetic data basically answers the question, to your satisfaction. To where you don’t need to look at non-genetic-

Peter Attia

Not alone. I think of it as the genetic data, coupled with the pharmacologic data, coupled with the mechanistic data, give me a high enough degree of certainty, that I am willing to act in a certain direction. Remember, everybody, me, you, whoever’s listening to this, they have to make a decision.

Dave Feldman

Sure.

Peter Attia

Indecision is a decision. So, when you showed up with the hemoglobin A1C of 6.1, did you have type two diabetes? Nope. Your doctor said, “Hey, I’m cool just waiting.” But you said, “No. Indecision is not a decision any more, I’m going to do something about it.” Because, presumably, you said, “Look, I have a family history of this. I think I have a sense of what the progression of it is. Quite frankly, I don’t want to wait until I have this disease to do something about it.” So, you decided indecision was not a viable decision.

Sometimes indecision is a reasonable decision. But, the point is, people have to understand they are making a decision whatever they decide to do.

Dave Feldman

Absolutely. Well, and for what it’s worth, as I say outside of here, and as I’ll say on this podcast, as I actually just said it, the speech, I don’t know if you saw the one that I did from last month. I told people, I prefer they not be echo chambering. I prefer they find everything that challenges from every side. So, with that said, going back to the lean mass hyper-responder, you would say, given what you know right now, given everything we’ve just talked about, that they are at high risk of cardiovascular disease. Would that be correct?

Peter Attia

I’d want to know more data. But, yes. If everything … If I didn’t know anything else other than-

Dave Feldman

Let’s say all cardiovascular risk markers say, LDL of 200 or higher, LDLP of typically 2,000 or higher, everything else is just pristine perfect, like CRPs at the floor, their LPPLA may be-

Case Study Talk

To my delight, Peter had a lab to chat about…

Peter Attia

Let’s look at this patient here. So, we’ll link to these labs. I asked this patient, this is a patient I saw last week. So that the only reason I printed this up, because I see this so often, but I’m like, “Let’s just get the last one.”

This is a gentleman who’s been on a low carb diet for a couple of years, is achieving amazing success with it. He’s a new patient to me, but he’s been around the block on this stuff before, and he’s got an amazing history of his labs going back many years. I’ve seen what he looks like on and off all of these therapies. On and off drugs, et cetera. He’s one of these guys where, across the board, looks fantastic, right? His glucose disposal is remarkable, his insulin levels are very low, his c-reactive protein is 0.3. Everything looks good. Read off some of his numbers, just for the folks, Dave. He doesn’t quite meet your lean mass, because his trigs might be a bit higher, but, talk to me about this guy’s numbers.

Dave Feldman

So, total cholesterol is 504.

Peter Attia

Is that high?

Dave Feldman

I know what you’re doing there.

Peter Attia

No, I’m just kidding.

Dave Feldman

I get this all the time where somebody sends me just that number.

Peter Attia

No, no. Okay. Go ahead.

Dave Feldman

Total cholesterol 504, LDLC direct, and it’s worth emphasizing just real quick for the listener, when they say direct, it’s very important to notice that, because usually, LDLC on a typical lab is actually calculated through the Friedewald Equation. So, when it’s direct, that actually is a direct measurement. And that matters for remnant. Hope we’ll get a chance to talk about that.

Peter Attia

We will talk remnants for sure.

Dave Feldman

So, LDLC at 362, HDLC at 94. Triglycerides at 125. The very first question I would ask if somebody was sending this to me is whether it was fasted or not?

Peter Attia

Yeah, this was. But, I’ve gone back and looked at all of his other trigs, and he actually, normally, does reside below about 70.

Dave Feldman

Oh, he does. Okay. So he would be typical for a lean mass.

Peter Attia

Yeah, he might have just eaten dinner a little too late, or something. I’m not sure what was going on.

Dave Feldman

Do you want me to keep going on the particles?

Peter Attia

Yeah, hit the particles.

Dave Feldman

So, Apo-B is 283? That actually is a little higher than I’m used to seeing. LDLP is about 3,500. Small LDLP is at 1,483. Small dense LDLC is at 47.

Peter Attia

All right, so we’ll just stop there and come back to it.I’ve told you that everything else on this guy’s looks pretty good. Is this guy at risk?

Dave Feldman

Well, I’m actually looking ahead, because I would have cared about these other markers. That could indicate inflammation, so, for example, the fibrinogen is very high. LPPLA2 is above 600. I don’t … In fact, I think I just Tweeted about this recently. I don’t know that I’ve seen an LPPLA2 above 300 or 400 of the labs that have been sent to me. I don’t get a chance to interpret oxidized LDL, but you have the LDL as above 135. So, I would say by this lab, as it looks, I would be concerned about the triglycerides, I would ideally want the triglycerides to go down.

So I have to concede, this was an awkward moment. I realized Peter wanted to zero in on whether I’d think the high LDL was an issue. But the whole profile matters. When we see LDL cholesterol levels that high here on the site, probably 90% or more it will end up being a LMHR and I’d fully expect the triglycerides will be below 100 at least (and usually they are below 70). So this profile already didn’t jive with the patterns I’m used to seeing.

The elevated Lp-PLA2 also set off my spidey sense. I’d wanted to know more about their situation, eating habits, and/or possible symptoms of illness.

So I followed up with a lot more Q&A I won’t list out here. We ultimately got to Peter’s key point…

Peter Attia

So, his cholesterol synthesis is through the roof, and his cholesterol absorption is quite high as well.

Dave Feldman

Are these affordable tests? Because I would definitely want to turn these around to the existing group of lean mass-

Peter Attia

I’m sure, the cash cost on these is not onerous.

But, my point is, I think that the explanation for this phenotype is the up-regulation cholesterol synthesis from the saturated fat. I don’t think this is an energy issue per se. I think this is a sterol regulated binding protein issue, or some sort of regulatory path around what the body is doing with ketones and/or saturated fat.

So here’s the thing — technically speaking, my and Peter’s theories aren’t really mutually exclusive. It’s quite possible this is energy trafficking and there’s higher sterol production overall. The modification I’d make is that this production would likely be dynamic in my model.

Peter went on to discuss a case with Dayspring and some further observations he’d made since.

Peter Attia

Bringing it back to this idea of genes, we might really be dealing with a subset of people, these hyper-responders, whoever, whatever percentage of the population they are, who are the people who are susceptible to this. Because you are not gonna find a leaner person, exercising harder than I was when I went on a ketogenic diet. I never had this response.

Dave Feldman

But there is a distinction that I tend to find and this is Occam’s razor. Again, more theory. I’m actually gonna be testing this myself in the next series of experiments that I’m doing. There is a difference between those people who are doing things like say endurance running, and weight lifting, or resistance training. In that, I think there is a greater overall gradient of receptor-mediated endocytosis for muscle repair and growth. I could be wrong about that, but I’ll be very curious to see if that turns out to be the case when I’m doing it myself.

Two things to mention real quick to the reader…

One — I have since completed that experiment and I was quite pleased with the resulting data! Indeed, it appears intensive resistance training (when everything else is tightly controlled) does reduce LDL cholesterol as predicted. Whether this is as I hypothesize to be receptor-mediated endocytosis on the part of the muscle tissue… well, that’s a bit harder to prove directly.

Two — If there’s anyone I’d expect to have lower LDL cholesterol due to this theory, it would certainly be Peter Attia! He’s no stranger to athleticism with resistance training! Check out this video: Peter Attia Tire flipping, jumping pull-ups, and other fun things you can do without carbs. So yes, I’m rebutting Attia here by slapping him with a fat compliment at the same time.

Do Muscles Endocytose LDL Particles?

This next part gets a bit long, but I think it’s a good read.

Peter Attia

Sorry, a greater amount of endocytosis of which lipoprotein, and for which product?

Dave Feldman

Of LDLP in particular.

Peter Attia

Into muscles?

Dave Feldman

Yup.

Peter Attia

For what product?

Dave Feldman

For repair and growth.

Peter Attia

You’re saying that in these people, they’re relying on their LDL for cholesterol delivery to the muscle?

Dave Feldman

Well, and phospholipids and just about anything else that would be inside of an LDL particle. There is existing studies that are out there, as far as those people who do a lot of weight training will also see LDLC and, this is why I’m saying it’s completely theoretical. I’ll actually be testing this myself over the next few weeks. Because I’m actually gonna be eating too, a very fixed diet, fixed sleep schedule, fixed everything. Then I’ll actually be introducing basically, any way in which I can get my muscles sore in a very fixed fashion, I can then turn around this data. If the hypothesis is true, I would expect that my LDLC, my LDLP might change.

Peter Attia

But, I’m confused. Why is the runner’s muscle more demanding than the weight lifter’s muscle? Or vice versa.

Dave Feldman

The other way around. That I would see the weight lifter actually seeing a difference. Because I think there’s more use of the product of LDLP directly by the cells. I may be wrong about that.

Peter Attia

But, what’s the evidence that that’s happening?

Dave Feldman

The evidence as far as … The keto gains groups. I’m sure you’ve heard of them?

Peter Attia

No.

Dave Feldman

There’s a ketogenic group, that’s keto gains, there’s not as many lean mass hyper-responders that come out of that group. They’ll tend to see their LDLC go up, but not as pronounced as those people who are say, runner-types, or aerobic-types, or even people who are doing yoga. There seems to be actually, a more pronounced difference of higher LDLC, depending on how much you’re doing resistance training, or anaerobic training.

Peter Attia

Yeah, again, I’m not aware of any evidence to suggest that the muscle is relying on LDL for delivery of anything. Including energy.

Dave Feldman

I’m not so sure about it on energy. What I’m thinking about is in terms of just raw material. I mean, as far as damage that can happen to, for example, the membrane of a cell. I realize this is kind of a key difference between us, is that your sense is that effectively, anything that the cell is gonna need, it can basically synthesize on its own, right?

Peter Attia

No, I think my sense is that … Occam’s razor would at least have me start from a place of plausibility. And I’m just not aware of any data that suggests that LDL is functioning to do this.

Dave Feldman

What’s the value of non-hepatic receptor mediate endocytosis from your perspective?

Peter Attia

So, you’re talking about very specifically, the little bit of LDL that gets out of circulation, either with or without a receptor to non-hepatic tissue?

Dave Feldman

Yes.

Peter Attia

My sense is the most important value of that would be to tissues that need more cholesterol to synthesis hormones.

Dave Feldman

But specifically cholesterol and not the phospholipids or anything else that-

Peter Attia

I think the phospholipids probably may be more delivered through others. Certainly, the VLDL delivers far more phospholipid than LDL. But, LDL is really a custom built package for cholesterol. If you look at how many cholesterol molecules fit inside and LDL particle, versus even an HDL particle … Remember, the HDL is the general of RCT. Yet, it can still only carry about 50 molecules of cholesterol. The LDL particle can carry 1,500 molecules of cholesterol. That’s staggering, again, when you consider the size of these things, right? It’s tailor made for that. That is largely conserved.

I don’t want to get us too far in the weeds, but I actually did a very interesting kinetic experiment many years ago. I did three blood tests every day for three days. Like the full NMR panel, but this is with kinetic. So, this is not commercially available. So, what you’re looking at is my ability to track, you’ll  have to lay it down, because I barely remember what I did, but this is pre-work out, immediately post-workout, four hours later, looking at my LDL particles, my VLDL particles, my HDL particles, both in terms of their cholesterol and triglyceride content.

Dave Feldman

So, you see them going down yourself?

Peter Attia

I don’t see any change in the cholesterol content. It’s minimal change in cholesterol content, right? What I think you see here is, “Yeah, wow. Under really periods of super high intense exercise, I actually did take some triglycerides out of this.”

Dave Feldman

Right.

Peter Attia

Minimal out of here. By the way, this backs up Garvey’s data, which is, there’s virtually no way to distinguish what’s going on at the VLDL level. We can’t tell what a remnant here, or what’s not a remnant. I apologize for the listener, we’re looking at a chart, but we’re gonna link to it, so you’ll see it. We’re basically talking about this idea of how much movement of cholesterol is going into, and out of, the LDL particle under these extreme conditions. I just did different types of workouts. So, on this day I did a crazy high intensity interval training. On this day, I did a crazy intense swim.

And I think on this day was the hardest workout of them all, was a crazy intense bike ride.

Dave Feldman

And the listener can’t see this, but I’m smiling ear to ear. It’s almost as if you knew I was gonna-

Peter Attia

Well, I thought you would appreciate … I forgot I did this. I did this six, seven years ago.

Dave Feldman

That’s fantastic.

We chatted a little bit more about the experiment after that.

Next part: Guesting on the Peter Attia Drive (3 of 5) – Remnant Cholesterol, Craig Moffitt, Fasting

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