Knife Down

Surgeon Reacts to the KETO-CTA 'Scandal'

• Lily Johnston, MD MPH • Season 2026 • Episode 49

Share episode

Use Left/Right to seek, Home/End to jump to start or end. Hold shift to jump forward or backward.

0:00 | 32:54

The KETO-CTA trial got retracted this year, and most of the internet treated it like a takedown. The authors pulled their own paper because they found real errors in the analysis. That took integrity. I react to how other creators have covered this retraction, walk through what the errors actually were, and make the case that watching scientists correct themselves in public is what good science looks like.

📚 STUDY DISCUSSED
Soto-Mota A, Norwitz NG, Manubolu VS, Kinninger A, Wood TR, Earls J, Feldman D, Budoff M. Longitudinal Data From the KETO-CTA Study: Plaque Predicts Plaque, ApoB Does Not. JACC Adv. 2025;4(7):101686. PMID: 40192608. https://pubmed.ncbi.nlm.nih.gov/40192608/ (Retracted Publication)

Expression of Concern: "Plaque Begets Plaque. ApoB Does Not: Longitudinal Data from The KETO-CTA Trial" [JACC: Advances, Volume 4, Issue 7, July 2025, Article 101686]. JACC Adv. 2026;5(3):102607. PMID: 41906601. https://pubmed.ncbi.nlm.nih.gov/41906601/

▶️ WATCH NEXT
Is Ezetimibe the Secret to Preventing Dementia? Surgeon Reacts to @nicknorwitzMDPhD: https://youtu.be/Rzz2g9gRL_8
Is Lower LDL Actually Better? New Research Has an Answer: https://youtu.be/Q2lvd9ND7rA

⚕️ DISCLAIMER
This channel is for education, not medical advice. I'm a board-certified vascular surgeon, but I'm not your surgeon, and nothing here replaces a conversation with your own physician.Sign up for more information on my own practice here: https://corsighthealth.com/

High Quality 3rd-party tested supplements at Fullscript (10% discount): https://us.fullscript.com/welcome/ljohnstonmd/store-start

Other tools for optimal health (note these are affiliate links):
Home BP Cuff: https://amzn.to/49Cq7rh
Sonicare Toothbrush: https://amzn.to/3KllfMS
WaterPik: https://amzn.to/4894Xi8
Intake Breathing Nasal Support: https://amzn.to/48dfQQ1
Personal Blender: https://amzn.to/4pyNGGl
True Nutrition Protein: https://oken.do/q2xzqeqw
Glass Meal Prep Containers: https://amzn.to/4ocEPJ2
Sleep Mask: https://amzn.to/48fSJV5
Air Purifier: https://amzn.to/4puzTQZ

___________________________
🧬 About Dr. Lily Johnston
  
Dr. Johnston is a double board-certified vascular and general surgeon in San Diego, specializing in metabolic and cardiovascular prevention. She’s the founder of CorSight Health and a passionate advocate for reimagining how medicine approaches chronic disease.

SPEAKER_00

This has been in my watch list for a little while. This is Talking with Docs, Dr. Broad and Dr. Paul. They are going to talk about the keto CTA trial. Some of you have asked me about it. I haven't done a whole video on it, but I really wanted to see what Talking with Docs was going to say, especially about the retraction. And I have a little inside knowledge about this. So let's watch and see what we get. If you're new here, I am Dr. Lily Johnston. I am a board certified vascular surgeon. I also specialize in cardiometabolic medicine. So hopefully you will never need me as a surgeon.

SPEAKER_02

So a study came out last year that showed that people on a keto diet that had really high cholesterol didn't have a problem with cholesterol.

SPEAKER_01

Wow, interesting study. It was retracted. What? Gone, taken.

SPEAKER_00

So this is an interesting video because I know Dave Feldman and I have been listening to him talk about the keto CTA trial for a while, a few years, as it has been ongoing, as the results have come out, and as they have had some issues with the data analysis that was done, especially from Clearly, which is one of the several companies that they have used to do an AI overlay for research purposes in this trial. So let me be clear that the paper was retracted at the request of the authors due to concerns over the quality of the Clearly data analysis. Nothing that the authors did, but their inability to get clearly the company to reanalyze the data and have some quality control in place with the results that the authors believed were, and now in fact know are not quite right. We'll get into that in a little bit. Let's see what else talking with docs have to say about the study.

SPEAKER_02

Out of the body of science. Okay, stick around. Welcome to Talking with Docs and Dr. Brad Meaning. I'm Dr. Paul Zalza.

SPEAKER_01

Now, a retraction of a scientific article is very rare.

SPEAKER_02

So we looked it up. Two to five out of every 10,000 articles get retracted.

SPEAKER_01

Okay, the most famous one that comes to mind for me was the one that showed the um vaccinations cause autism.

SPEAKER_02

Oh, the gastroenterologist guy with the kids and all that stuff.

SPEAKER_01

That study was taken out of science. Hang on. I said no. Science giveth, and science taketh away.

SPEAKER_02

Right. And it gets taken away for a bunch of different reasons. Sometimes you learn afterwards, like, okay, maybe the interpretation was wrong, maybe the data was interpreted wrong, maybe there were actually full-on falsification or disclosures that weren't open.

SPEAKER_01

It's kind of a big deal because you can have a study that says something, then you can have another study that says something else. Right. And it's not retracted if both studies were done well. Agreed. Okay. But if there are real flaws with the methodology or the patient population, or if the author is just lied, then that study's retracted.

SPEAKER_02

But this study, there's people really excited. So people on keto dot are really excited, people on the super low carb thing were really excited. The cardiologist and the lipidologist were not super excited. So there's like, and they they have a lot of conflict. So what was the title of the article? Not that you can find it, because it's been scrubbed from the internet. Like if you hire like a company to make you know that office Christmas party photo go away.

SPEAKER_01

And that never will. That never will. So be careful. Um the study was called Longitudinal Data from the keto-CTA study. Plaque predicts plaque Apo B does not. And it was in the journal of the American College of Cardiology. Is that what it is?

SPEAKER_02

Yeah, so pretty G A C C Yeah, like a good journal. And in the title, pretty bold claim in the title. So that for me is always a red flag when you're like, wait a second, so this one study has taken away, you know, decades of scientific research, randomized controlled.

SPEAKER_00

It has not taken away decades of scientific work. This trial was focused very, very specifically on a phenotype called the lean mass hyperresponder. This definition was set out in the study methodology, and I won't recapitulate it here other than to give you a gist of who this was. But these were a very highly selected group of patients who were had very elevated LDL cholesterol as the result of going on a very low carbohydrate diet. But we knew that they had more normal LDL cholesterol levels prior to using a low carbohydrate way of eating. And they had low triglycerides, high HDL, and this very elevated LDLC that was the direct result of their ketogenic or very low carbohydrate way of eating because they had lab results and receipts essentially to show that that had happened once they started a ketogenic diet. So this is not everybody with elevated LDL cholesterol. This is a very select group of people who do not have any evidence of the metabolic syndrome, their triglycerides were low, their HDL, again, was high, and this was done very intentionally to really try and isolate out this particular group of people whose LDLC goes up on a ketogenic diet. This was not designed to undo the entirety of the lipid heart hypothesis, and many in the keto community would hope that this was the first step, perhaps, uh, in knocking that hypothesis down. But this is not everybody with elevated LDLC. It's just not. This was a really tightly controlled population, and the authors did that on purpose. So, and they would never tell you that the purpose of this study was to undo the entire lipid heart hypothesis. It was only to see whether, in this highly selected group of patients, was LDLC or APOB a predictor of plaque progression.

SPEAKER_02

Trials, Mendelian genetics to study to show that you know cholesterol and elevated APOB do correlate and potentially are causative in heart disease. I'm saying, oh, well, this one study is gonna take that away. So let's talk about the study.

SPEAKER_01

It doesn't pass the SNF test.

SPEAKER_02

Doesn't pass the SNF test. So this study had 100 patients.

SPEAKER_01

100 patients. Good follow-up.

SPEAKER_02

Very specifically picked because they're what are called lean mass hyperresponders. Right.

SPEAKER_01

That's kind of what I described you as.

SPEAKER_02

A lean mass hyperresponder. Wow. I feel like I feel like it's not a dig on the lean mass side. I feel like it's the hyperresponder that he's making fun of me. And I'm just joking. I resemble that remark. Resemble it. Irregardless. Did you notice people really thought irregardless was quite funny last time? Someone's like, please don't use that word. Um anyway, so 100 people, lean mass hypersponders. So you're like, well, what does that mean? So these are people who are on a ketogenic or a very ultra-low-carb diet, who are lean, who are fit, who have actually perfect sugar blood work and often are metabolically totally normal, but have very, very high LDL, like dangerously high LDL. And this is a small subset of population. These were picked because the authors were very interested in this group. They actually coined the term, interestingly. Yes. And they were big proponents of the keto diet, and they had wrote, I think, a cookbook and some other stuff. So it was kind of like a little bit trying to propagate their own beliefs, which I think it's normal to have some bias, right? You you do research probably on things that you believe in or stuff that you really believe against, you're trying to disprove it. But we all come with biases.

SPEAKER_01

First of all, these authors were from all over the place. UCLA, Harvard, New Mexico, Washington, they're from all over. Yes. Two, you've got a very unique subset, a sample size, a unique population. Right. And then in your title, you go in and put a generalization. Right. They're not representative of society. That sample size doesn't represent the normal population. Right. So you shouldn't put a generalized statement in your title.

SPEAKER_02

Agreed.

SPEAKER_00

So how I perhaps that's a fair criticism. I won't dispute that, you know, the idea of over-generalizing your findings is um perhaps a little unfair. I will say titles are pretty short and sometimes it's hard to get everything in there. Nobody knows what a lean mass hyperresponder is outside of the keto carnivore community, I don't think. So I don't necessarily blame the authors for not putting that there, especially in a journal as uh widely distributed as Jack Advances is. So, you know, it's a fair point. We'll say that.

SPEAKER_01

How does an article get published? Well, you write an article, you submit it to a journal. The journal then gets peers, other people, and I do this quite often. I'll get articles from journals, say, can you review this and tell us, A, is it publishable like it is? B, are there some minor changes that need to be made so this can be publishable? C, are there some major changes that need to be made that you did? Or do you chuck it in the garbage?

SPEAKER_02

Yeah.

SPEAKER_01

But you don't like when I get this article to review, I kind of you trust that the authors aren't lying. Like I don't go back and say, okay, give me all your raw data and let me analyze it. Not practical. No. So you kind of have to trust that people are telling you the truth, Matt. But that's the process. So it's a pretty and it's not just one reviewer that you send it to.

SPEAKER_00

I will also say if you are the author of a study and you are having your data analyzed through a you know business agreement with another company that is providing data analysis for you, you trust that the data that are coming back to you are appropriately analyzed, that whatever protocols you put in place, whatever quality assurance you had as part of your agreement, that has all been done. And that is not just like a reviewer will assume that the authors are giving them their results in good faith. If you are an author and you are a scientist, you are assuming and hoping that the collaborators you have that are providing you the analysis are doing so in good faith. That is the crux of what happened with the clearly portion of the data analysis of Keto CTA. A lot of the rest of the results that were done by QAngio and by HeartFlow still substantiate the original claim that Ape O B did not predict plaque progression in this study population. We'll get to that in a bit.

SPEAKER_01

Right? So it is there's a process, so it's kind of a big deal when something gets.

SPEAKER_02

And the other trouble is that humans are involved on both sides. Yeah. So the reviewers can make a mistake, the authors can make a mistake either intentionally or unintentionally. So there's a lot of potential for error.

SPEAKER_01

And then reviewers are arm length away. Like if I got an article that said that you wrote, then I'd be conflicted.

SPEAKER_02

Because you'd reverse stamp it. Yeah.

SPEAKER_01

And then I take it. Your crawly paper. That's right. So arm's length away reviewers, you know what I mean? Right. So the first thing that I see when I look at this is like, well, you've got a tight sample size of a certain group of people. Now you put a big general statement in your title.

SPEAKER_02

Right. So they had 100 people, they had baseline level blood work that showed they had elevated LDL A B, they had a CCTA, so a coronary CT scan angiogram. So better than a calcium score, which just says soft plaque. This is actually a very good or the gold standard test to assess the amount of plaque inside of your vessels.

SPEAKER_01

So plaque in your vessels makes the vessel smaller and that leads to heart attacks and strokes.

SPEAKER_02

And we talked about plaque, how plaque contains cholesterol. We don't have to get into a big discussion about is cholesterol the cause of it. It's a combination of things: cholesterol, inflammation, vessel damage, the triad.

SPEAKER_01

Right. So the punchline, what did they see correlating that?

SPEAKER_02

Wait, so then they did another test at one year. They followed these people for one year, and then they did another test, another CCTA. Um and what they showed is that having elevated APO B didn't necessarily mean that you got more plaque than someone that had a lower APO B in this group.

SPEAKER_01

Yeah. So they looked at the difference, the progression of plaque, and tried to correlate that with the levels of your APO B and control DL. And said, look, there's no correlation. It doesn't matter. How much you progress your plaque has nothing to do with what your levels are.

SPEAKER_02

They said the biggest risk was the risk of getting more plaque is if you had plaque, which also we know, right? We know that that's a thing.

SPEAKER_01

Um so I thought that was kind of like saying if you took a bunch of people who had lung cancer, god forbid you have lung cancer and you're a smoker, right? And then you looked at how many tumors you have in your lung or if it's spread, then you check again a few months later and say, Oh, look, it's spread. Let's correlate how much it's spread to how many cigarettes you have.

SPEAKER_02

Right.

SPEAKER_01

Doesn't matter at that point. And then you say, look, smoking doesn't cause cancer. It's having cancer causes cancer. Yeah. Like it's the same thing.

SPEAKER_00

So I'll push back on this just a hair. Because the authors actually will freely state, as they have uh publicly many times, that their findings here in Keto CTA do not negate the potential causality of LDLC or APOB in the formation of plaque. All they are saying is that the progression of plaque, much like the cancer analogy that uh Talking with Docs just gave, is that once you have it, the amount of APOB particles you have alone is not what's predicting progression in this specific population. Does that mean that at large it's not predictive? No. Does it mean that dropping APOB down with the medications or supplements or lifestyle measures that we have to do so would not reduce the amount of plaque progression? That is also not true. That doesn't mean, okay, let me say that again in another way. Just because having more APOB doesn't predict progression doesn't mean that reducing it below a threshold might not halt progression. Let me give you another analogy. Hormone-responsive cancers. So prostate cancer that is hormone responsive or breast cancers that are hormone responsive. To a first approximation, how much circulating estrogen you have doesn't necessarily talk a lot about how likely your breast cancer is to progress, but if it's hormone responsive, we are going to suppress your estrogen below that threshold so that no amount is getting to your tumor cells to feed the progression. Okay. It's not like we have to reduce it just a little bit. There's a specific threshold impact of estrogen or testosterone for prostate cancer. And unfortunately, for those patients to prevent spread of their tumor, we have to get it really below that threshold. And what is emerging in the science of APOB is for people who have known plaque, reducing APOB below a threshold, which the lean mass hyperresponders in this study never went below, will potentially help ameliorate the progression of plaque. That does not mean that it's necessarily the APOB, although in the aggregate, when we look at all of the studies, the amount of APOB lowering does track with the amount of reduction in cardiac events. So people believe the scientific community, the cardiology community believe that in fact the amount of APOB particle lowering is relevant, but it could be the ancillary, what we're calling pleotrophic effects, right? Some other things that come along with these interventions that may be helpful. So again, just because at a very high level, the amount of APOB did not predict progression of plaque does A, not negate causality for the formation of plaque in the first place, and B does not mean that dropping APOB down would not prevent progression or at least slow progression for these patients.

SPEAKER_02

Right, because the guy that had five cigarettes didn't get his cancer didn't get worse than the guy that had 25 cigarettes.

SPEAKER_01

So it's too late, you missed the boat, that ship has sailed. You can't correlate it to those blood markers.

SPEAKER_02

Right.

SPEAKER_01

How about whether or not you have the plaque correlate that to the blood markers?

SPEAKER_02

Right. And so so what happened was people in the keto community were really excited, right? And I think um first thing I'd say about keto is like all keto dyes are not the same.

SPEAKER_01

No.

SPEAKER_02

Right?

SPEAKER_01

So the other thing was to say there were some issues with the third party that was doing the CTA analysis. They wouldn't release their data and there's some methodology studies. Sorry, so there's some other issues.

SPEAKER_02

Not that the test wasn't good or accurate, but yeah, some with the data. Oh, the other thing too is that they're just measuring um blood levels and the CCTA. They were not looking at it if they they didn't comment at all if they had a heart attack. Yes. If they had a stroke. Obviously, no one died because they had 100% follow-up, which is good.

SPEAKER_01

And the follow-up period is quite short. It was only a year. One year. So these are some. And no control group. There's no control. So these are some of the problems why it was retracted. Okay, now sorry to interrupt you.

SPEAKER_00

You were so none of those things were he I I think was about to say those are the reasons it was retracted. Those have nothing to do with the retraction, right? All of that was known at that time that the study was submitted, meaning there was no control group. We knew that. Uh, they had the short-term follow-up. That was again designed as part of the trial, right? Repeating the CCTA at one year, because God forbid there had been rapid plaque progression as the result uh or correlated with APOB. We would want to know that as soon as possible and tell the participants that. So all of this was very intentional on the part of the authors. And I'm not here to defend the keto CTA study. I am here to try and be honest and factual about what has happened and not demonize the very commendable pursuit of science that has happened, in my opinion, uh, here with these authors and with this trial, because I do think it was a good faith effort on the part of the authors to answer an important question. And I am saddened when it becomes so politicized, right? This idea that science is controlled by who sits on editorial boards and who knows whom, and these relationships, you know, uh, these are not necessarily blinded when they're peer-reviewed. So people know who wrote them, people know what's happened, and a lot of science can get steamrolled or shuttered by these political infights where there are controversies or conflicts between people or between organizations or between philosophies and schools of thought. This is the the really seedy side of evidence-based medicine, or as some people call it, eminence-based medicine. And I want to, again, just commend Dave and Dr. Sotomoda and Dr. Norwitz and all of the team that um Dr. Budoff, who came together to try and ask and answer a question with basically no classical funding. I'm not sure you have any idea how hard it is to take a hundred people, fly them out to the specific scanner, get them scanned, follow them for a year, and do it again. And this was all funded by community people, right? You and me or whoever was donating money to the Citizen Science Foundation to do this. It wasn't from an NIH grant, it wasn't from industry or pharma or anybody else. This was grassroots-funded science. And that should warm your heart, even if you don't care about keto, even if you don't care about APOB, even if you think it's full of crap. I think this is a wonderful expression of curiosity and a desire to try and answer an interesting and important question.

SPEAKER_01

We're gonna say the keto people are.

SPEAKER_02

So keto people were excited. So the trouble is all keto diets are not the same. So the principle of keto is if you reduce your carbs, this can help your blood sugar, which certainly elevated blood glucose, is a problem for a lot of different metabolic conditions, and potentially your triglycerides, and potentially and actually these people actually have low triglycerides, ironically. The lean mass hypresponders have low triglycerides, um, which can contribute to LDL. So a lot of people are really happy. But so one person could be keto and say, I take eat zero carbs, but I eat a lot of a lot of animal products that are high in saturated fat. So if you're like on the bacon, butter, cheese team, yeah, that's different than the keto who say I'm having more chicken breasts, more healthy fish, and maybe they can have some carbs, uh, but not refined carbs. So all keto is not created equal. There certainly there are ways to do a keto-style diet that can be very healthy.

SPEAKER_00

Low carb diet. Right. So I completely agree with this. Ketosis is a physiologic state that reflects the production of ketones from the liver that are detectable in your blood. That is nutritional ketosis. We can do that with fasting, we can do that with reduced carbohydrate intake, and how we choose to eat for the remainder of the macros that we intake, including proteins and fats, is highly variable. But I know people who are minimal animal products who achieve therapeutic ketosis, and people who are only animal products who achieve therapeutic ketosis, and people who are only animal products who are not in a ketogenic state. The diet that was um trialed here, what, you know, they didn't measure ketones necessarily. And so um actually, I don't know that that's true. They might have. In any case, the expression, you know, not all keto is created equal is absolutely true. And there are many, many ways to skin that cat. And the question is, what are you trying to achieve? Are you trying to improve blood sugar? Are you actually trying to get a higher level of blood ketones because that is important for uh intractable epilepsy or mental health concerns or maybe a cancer, a malignancy? There are all kinds of reasons to shoot for higher ketone levels. And how you get there is highly variable, and I think it matters, but uh that's not something that we talk a huge amount about in the community, partially because moving from a standard way of eating with a lot of refined and processed crap to anything that is uh better is a huge step for so many people. And that is the place to start. And beyond that, once our hunger is controlled, once cravings are controlled and food addiction is controlled, right, then we can talk about how we tweak, how we evolve our patterns to the most helpful approach that works for us as individuals.

SPEAKER_02

A low carb diet. And when we say low carb, it's not because carbs themselves are evil. That sweet potato is not evil per se, but really we could probably agree that refined, highly processed carbs. Regardless of their form are bad for you. They're made to be hyperpalatable. You overeat them and they cause a lot of bad things to happen. Yeah, true. And someone's gonna leave that comment. Yeah, I read the one comment today that said, just if you eliminate everything, you don't really live longer. It just seems like because your life sucks, or something like that. And I'm like, I'm like, I agree with that. That's kind of fair.

SPEAKER_00

That's what my dad tells me every time I recommend that perhaps he not eat or drink quite so much. He says, I yeah, I'm in my 80s. It's not gonna actually make me live longer. It'll just feel longer. I'm good.

SPEAKER_02

Okay, so at the end of the day, what happened? So a year later, about nine months later, then a bunch of people were looking at it, and some of the authors were involved in the retraction, and they're like, you know what, we're not really comfortable with the conclusions that were made based on this study. It's not, it's not that the LDL levels were wrong. It's not that the imaging studies were wrong, but that to apply this conclusion to say that if you're on a keto diet and you're a lean mass hyporesponder, that your LDL and your AP levels don't matter. Because they do matter. 100%. Maybe they didn't matter for those hundred people over the course of one year. Um, but the way that it was interpreted was A, not accurate, not applicable to a general population, and definitely not a safe way to advise these people to live their lives.

SPEAKER_01

Yeah. So you take away the article, say nope, sorry.

SPEAKER_00

Um that's really not why it was retracted. It was retracted to the best of my knowledge, right? I'm not an author on this paper. Again, I'm not here to defend it, but my understanding of the retraction had everything to do with the analysis that was done by Clearly that showed every single person in their group had progression or uh null, but there was no regression of plaque in the clearly analysis. And statistically, that's an anomaly, right? Statistically, you expect to see some noise in your uh next test. And so there should be some progression, there should be people who are stable, and there should be some regression. If you see none, that means there's something that's not quite right with the analysis. What was even more interesting was that we not we, what I'm not involved in this. They had a number of participants in the study. So when you go get the CCTA, that is the scan, right? The scan has the imaging data, though those are raw data, and that is available, and that was what was sent to Clearly. It was sent for QAnGio analysis, it was sent to HeartFlow for that analysis, but the scans are the scans, as doc as Dave Feldman likes to say. The scan is the scan is the scan, and it is the truth. And so HeartFlow shows progression and regression. QANGIO shows the same, and that is reassuring, right? Those two are concordant, clearly had a different um data set and and or at least a different uh interpretation of what happened to the participants. Then what happens? The participants who were in the study, they get the results from the study of their progression from time zero to time one. And study says they have progressed 10%. Then they take their own data, they get the CDs from the UCLA imaging lab, and they uh go to their doctor and say, Hey doc, will you send this to Clearly? Send my time zero scan and my time one scan and have Clearly analyze it independently outside of the study. We're not even gonna like no study. We're just I'm an independent person out here living in the world. So they send those scans in and they get different answers. So the original study says the study data say 10% progression, but the submitted by the doctor's office says no progression. No, stable. And this has happened for multiple participants. I think eight or 10 participants have done this and gotten their CDs from the study, sent them in independently, and had different answers. So this is very concerning. And the authors went to the research team at Clearly and said, hey, we have concerns about how these data were analyzed. We think that there's a problem here in the process. Will you reanalyze? Will you go back to square one? Will you go through this quality assurance process and help us understand what happened here and like see if we can reanalyze it? Because look, we have conflicting information. We know that you're not giving the same answer with the same scans based on the same exact pictures. You're getting two different answers. That's not okay. So it's not that the whole conclusion of the study was wrong because the heart flow and the QANGIO are still saying the same thing and they are concordant. There is some progression, there is some regression, probably that's below the threshold of minimal detectable change for the study. So perhaps it's just noise. But there was still no big aha, guess what? APOB correlates with plaque progression. No, we have those data. They are the same. What has changed is this sense that the clearly analysis is unreliable and should not live out in the world as evidence of anything because we don't know what those data are. And I think that's the important take-home message for you know a little inside baseball that I'm aware of about what happened to that trial and what the data analysis problems were.

SPEAKER_02

Yeah, so it's gone. I can't find it.

SPEAKER_01

It's gone.

SPEAKER_02

Maybe you can find it in like the maybe in the black web or the dark web.

SPEAKER_01

Yeah, I'm sure it's kicking around somewhere.

SPEAKER_02

So when you go looking on the dark web for whatever you're looking for, you might still be.

SPEAKER_01

That's right. All right. So there you go. That article is gone. Keto diets used with caution. Like you said, there's different kinds. Is it like a carnivore diet? Is that like an extreme keto diet?

SPEAKER_02

I think technically, uh if you're a rigid carnivore, that would be a very strict keto diet. Yeah.

SPEAKER_01

So uh they have the role. I mean, they used to be used to manage diabetes before we had insulin. That's right. Getting people into ketogenesis. Yes. But in general, um what the conclusions of that article are now taken away from science. Don't exist.

SPEAKER_02

Right. Don't think that if you're doing this diet and you have elevated LDL or April B, that it is not an issue. You should definitely discuss it with your family doctor. Discuss whether or not you require medication, whether or not you should tweak your diet, whether or not you just need to be followed. But but yeah, I think there's a lot of things. It just goes to show that taking one study out of consciousness. This happens online all the time. Yeah. And this, oh, that was the other criticism, too, is that these people were involved in that community, the keto community, and they released a lot of stuff, essentially even before, almost like hyping it up and promoting it in a dangerous and arguably irresponsible way. And that's that's the trouble. We want to try to stay as objective as we can. And just like our channels, we just try to give you the information, you can decide what you do for yourself. We just don't want you to make a decision based on something that's not factual or accurate.

SPEAKER_01

And plus, I thought this was just a neat example of how a study gets taken away. Yeah, you know what I mean? We don't see it that often. So it's kind of cool to just highlight. Look, science does have some guardrails that try and make sure that we're moving towards the truth. Because if something's an outlier or something's wrong, science tries to correct itself.

SPEAKER_02

Now, you know, leave a comment if you are on a keto diet, if you have high cholesterol, if you are a lean mass hyper responder, leave a comment if you like this video. Please like it, subscribe to our channel, share it with someone that maybe has been piping off about this study.

SPEAKER_01

Remember, you are in charge of your own health.

SPEAKER_02

See you next time.

SPEAKER_00

So I will just say that the again, this was not a gotcha, right? This was not the scientific community coming in and saying, this was a terrible study. We're not gonna stand for this. Off with their heads, right? And retract the whole thing. This was the authors having concerns about data they were given or analysis they were given in good faith that they ultimately discovered did not meet their standards for quality or quality assurance. And they were concerned that that perhaps was a misrepresentation, and they want the opportunity to bring this back with the best, highest quality data and give the most accurate answer. So I just would push back on the mischaracterization of what happened. This was not fraud, this was not malfeasance or somebody, you know, acting badly, uh, at least on the part of the authors. And I I hope that this is not taken as proof that the conclusions all get thrown out. I don't think that's fair. And I also don't think it's fair to say that if you're a lean mass hyperresponder, your APOB is totally irrelevant if you have a great deal of plaque. There were a number of things about this study that were interesting, most of which having to do with a pretty low plaque burden in these patients overall. So when they were discussing the amount of plaque progression, there was a lot of conversation about how much plaque progression versus uh or what was relative versus what was absolute. So there were critiques of the study that said the degree of plaque progression was rapid and much higher than other cohorts where we have followed CCTA over time. And the author's response was it's relative, but if you look at the absolute plaque progression, many of these people had low levels of plaque at baseline, and then they went from a low level to a slightly higher low level. And it relatively looked like a lot, but on absolute terms, it wasn't very much. So this is an evolving area, and I just want to be fair and cautious and allow for people to raise questions and have them try to be answered. That is the heart of science. We are all doing our best to interpret things with an appropriate amount of skepticism, not too much, and and but not, you know, buying everything uh whole hog, right? There's so much contradiction in the literature, especially around lifestyle interventions, especially around nutrition. And the lipid space is continuing to evolve. We are continuing to understand about the impact and who is impacted. I don't think that the effect is necessarily universal or uniform. So stay tuned as we get more information. I do believe we will hear more from the keto CTA authors as time goes on and more analysis comes down out of that trial. I hope that they will do a longer follow-up. I know it's been discussed, and uh I know they have some other projects in the works. Let me know what you guys think of that below. I am gonna go back to that and give that video a like. And until next time, take really good care.