You switched to a ketogenic diet. Your triglycerides dropped. Your HDL went up. Every marker of metabolic health improved. Except one: your LDL skyrocketed.

According to the standard story, that means you're a ticking time bomb. High LDL equals clogged arteries equals heart attack. That story shaped public health guidelines, statin prescriptions, and the careers of thousands of cardiologists. But a groundbreaking study just found something that doesn't fit the script: in people with sky-high LDL on keto, plaque progression had no association with LDL cholesterol. None. Not even with ApoB.

I'm Dr. Ford Brewer, a preventive medicine physician trained at Johns Hopkins, with over 40 years of clinical experience. I've spent decades measuring plaque directly in patients, and I can tell you: what drives plaque growth is more complicated than a single cholesterol number. The standard story is neat and simple. Biology isn't.

In this article, I'll walk you through what the KetoCTA trial actually found across four independent analyses, why one AI company's data disagrees with the other three, what actually predicted plaque progression, and what this means for you if your LDL is elevated on a low-carb diet.

The Mechanism: What Actually Drives Plaque Growth

Most people think high LDL cholesterol drives plaque into the artery wall in a simple, dose-dependent way. More LDL equals more plaque. The real picture is more complex than that.

Here's what the KetoCTA trial data shows. Plaque progression was predicted by one thing: how much plaque you already had. Not by LDL. Not by ApoB. Baseline plaque burden was the strongest predictor of future plaque growth. The more plaque at baseline, the more plaque at follow-up. This pattern held across four separate analyses by four independent teams using different methodologies.

The mechanism that likely explains this: existing plaque creates local inflammation, endothelial damage, and hemodynamic stress at the lesion site. That local environment recruits more ApoB-containing particles into the wall, regardless of what's circulating in the bloodstream. Plaque begets plaque. The neighborhood is the problem, not the traffic passing through.

This doesn't mean LDL is irrelevant to cardiovascular disease broadly. ApoB lipoproteins are part of the causal pathway of atherosclerosis. But it does mean that in metabolically healthy people on ketogenic diets, an elevated LDL number alone may not tell you whether your arteries are actually in danger. What tells you? Direct imaging. Measuring the plaque itself.

What Is the KetoCTA Trial?

In April 2025, Dave Feldman, alongside Dr. Matt Budoff and Dr. Adrian Soto, published the KetoCTA trial: "Plaque Begets Plaque. ApoB Does Not." This was a study of lean mass hyper-responders, people on ketogenic diets whose LDL cholesterol rose dramatically, often to levels above 250, 350, even 450 mg/dL.

Participants had two CT angiograms one year apart. CT angiograms are the gold standard for detecting coronary artery plaque. They show soft plaque, calcified plaque, and mixed plaque in 3D throughout the coronary arteries.

The cohort was middle-aged, averaging around 55. They'd maintained elevated LDL levels for an average of 4.5 years before the first scan. If the standard cholesterol model were correct in a straightforward way, these people should have been building plaque aggressively for years.

What Most People Miss

This wasn't a small pilot. It involved roughly 100 participants with LDL levels beyond one in a thousand in the general population. Four separate analyses were performed on the same imaging data. That's unusual. Most studies get one read. This one got four, using different teams, different methodologies, and different AI platforms. That redundancy is what makes the findings hard to dismiss.

Four Analyses, One Core Finding: No Link Between LDL, ApoB, and Plaque Growth

The four analyses performed on the KetoCTA data:

  • Semi-quantitative analysis (Dr. Budoff's team): Blinded expert cardiologists scoring plaque at 15–17 predetermined checkpoints through the coronary arteries, grading from 0 (no visible plaque) to 3 (severe plaque).
  • Cleerly analysis: AI-guided quantitative plaque measurement.
  • HeartFlow analysis: AI-guided quantitative plaque measurement by a separate company.
  • Qangio analysis (Medis): The pre-registered methodology for the study. Also quantitative.

All four analyses agreed on the two major findings:

  • Baseline plaque was the strongest predictor of future plaque progression.
  • There was no association between LDL or ApoB and plaque progression.

Three of the four analyses (semi-quantitative, HeartFlow, and Qangio) also broadly agreed that the majority of participants showed little to no plaque progression, with some even showing plaque regression, actual shrinkage.

What Most People Miss

Dr. Soto ran every subset analysis he could. People with positive coronary calcium scores only. People with the highest LDL only. The small group of rapid progressors only. In no subset, by any method of analysis, was there an association between LDL or ApoB and plaque progression. Three independent teams, three different methodologies, same conclusion.

*Question to Ask Your Clinician:*

"Given my LDL is elevated on keto, can we measure my actual plaque burden with a CT angiogram or coronary calcium score rather than just treating the number?"

Some People With Sky-High LDL Actually Showed Plaque Regression

This is the finding that changes the conversation. Among participants with LDL levels most doctors would consider dangerous, a subset showed verifiable plaque regression. Their arteries actually improved over the year between scans, despite sustained, extremely elevated LDL.

This was confirmed across three of the four analyses (semi-quantitative, HeartFlow, and Qangio). Only the Cleerly analysis showed zero regressors.

Dave Feldman predicted this outcome. He knew that in any middle-aged population, some people will progress, some will remain stable, and some will regress. The critical question was whether regression could exist in the presence of very high LDL. The answer is yes.

What Most People Miss

A small subset also showed rapid progression, as you'd expect in any middle-aged cohort. This is why blanket reassurance is dangerous. Some people with high LDL on keto are building plaque. Others aren't. The only way to know is to look. Not at the cholesterol number. At the artery itself.

*Question to Ask Your Clinician:*

"If my LDL is high but my metabolic health looks good, what testing will actually tell us whether plaque is progressing?"

Why the Cleerly Data Stands Alone

One of the four analyses tells a different story. The Cleerly AI reading showed higher rates of plaque progression across the cohort, with no participants showing regression. Critics seized on this to argue the study actually proved keto was dangerous.

But here's what happened after publication. Once the raw imaging data was available to the research team, Dave Feldman found anomalies in the Cleerly data set that didn't match the other three reads. Specifically:

  • Cleerly showed zero regressors across the entire cohort. The other three analyses all showed regression in a subset of participants.
  • In the Cleerly data, roughly 40% of participants had zero calcified plaque volume at baseline. At the one-year follow-up, nearly half of those developed detectable calcification for the first time. In a cohort that had maintained these LDL levels for an average of 4.5 years, having half suddenly convert in exactly the one year of observation is statistically implausible.
  • HeartFlow averages were similar to Cleerly's for many participants, but Cleerly's values were consistently higher in the second scan, like a fixed offset.

Feldman reported these concerns to Cleerly's Chief Medical Officer, who agreed to a quality control pass, essentially rerunning the scans to check for errors. Then Cleerly reversed course and refused. The company is reportedly preparing for an IPO.

What Most People Miss

Even the Cleerly analysis, the one that showed more progression, still agreed with the other three on the core finding: there was no association between LDL or ApoB and plaque progression. The disagreement is about the magnitude of progression, not about whether cholesterol predicted it. It didn't, in any of the four reads.

*Question to Ask Your Clinician:*

"When I get imaging done, how do I know the analysis is reliable? Should I ask about which platform was used to read my scan?"

The Bigger Question: What Does This Mean for LDL and Heart Disease?

This trial doesn't prove LDL is irrelevant. ApoB-containing lipoproteins are part of the causal pathway of atherosclerosis. But the relationship between circulating LDL levels and actual plaque behavior in metabolically healthy people may not be the simple, linear story we've been told.

Here's what concerns me most as a clinician: how much focus there is on LDL and ApoB when we know much larger cardiovascular risk factors aren't getting the same attention. Insulin resistance is a cardiovascular disease risk factor with hazard ratios far above LDL in every study that looks deeply into it. Poor metabolic health, chronic inflammation, and the lifestyle patterns that drive them are doing more damage in more people than an elevated LDL in someone who is otherwise metabolically healthy.

I have family members taking aggressive steps to lower their LDL because they've been told that makes them heart-attack proof, despite their poor metabolic health. That's the real danger of the single-number story. It gives people a false sense of security while the bigger risks go unaddressed.

What Most People Miss

The low-carb community ran with this study as proof you can ignore your LDL entirely. That's not what the researchers said. The researchers said: we're reporting what we found. No association in this cohort. Some people regressed. Some progressed rapidly. The takeaway isn't "ignore LDL." The takeaway is: measure the thing that matters directly. Don't assume a number on a blood test tells you what's happening in your arteries.

*Question to Ask Your Clinician:*

"Are we treating my cholesterol number, or are we treating my actual cardiovascular risk? How do we know which one is actually elevated?"

What Standard Care Misses (And the Testing That Actually Helps)

Here's the structural problem. Standard cardiovascular prevention treats a number, LDL cholesterol, and assumes the artery is fine if the number comes down. But this study found no association between that number and what was actually happening in the artery.

Meanwhile, the metabolic factors that likely do drive plaque in most people, insulin resistance, chronic inflammation, arterial stiffness, are not on the standard panel. Your annual physical checks fasting glucose and a basic lipid panel. Those don't catch the disease process early. They catch it late.

This is a structural limitation of primary care, not a failing of individual physicians. The 7-minute appointment and the insurance-reimbursed panel weren't designed for cardiovascular prevention. They were designed for disease management after disease has already arrived.

The testing that actually helps:

  • OGTT/IR — oral glucose tolerance test with insulin response. Catches after-meal insulin problems that fasting tests miss entirely. This is where early metabolic disease lives.
  • CGM — continuous glucose monitoring. Real-world blood sugar patterns across meals, sleep, and stress.
  • Lipid fractionation, including ApoB and small-particle LDL (sdLDL) — directly counts the artery-damaging particles. Standard LDL is an estimate. Useful in context, but not the whole picture.
  • hsCRP, Lp-PLA2, MPO — inflammation markers that predict plaque rupture. Inflammation is what makes plaque dangerous, not just plaque volume.
  • CIMT and coronary calcium scoring (CAC) — direct imaging of the artery wall and calcified plaque burden. And for the most complete picture: CT angiography, the gold standard used in this study.

The lesson of the KetoCTA trial is straightforward: if you want to know whether plaque is growing, measure the plaque. Don't guess based on a blood test.

The Bottom Line

Four independent analyses of the same imaging data, three of them broadly agreeing: in metabolically healthy people on ketogenic diets with sky-high LDL, plaque progression was not predicted by LDL or ApoB. It was predicted by how much plaque was already there.

A practical recap:

  • The KetoCTA trial found no association between LDL or ApoB and plaque progression across four analyses.
  • Baseline plaque was the strongest predictor of future plaque: plaque begets plaque.
  • Some participants with very high LDL showed actual plaque regression.
  • Three of four analyses showed little to no net progression in the majority of participants.
  • The one analysis that disagreed (Cleerly) has unresolved quality control concerns and the company has refused a re-check.
  • This doesn't mean LDL is irrelevant. It means a number alone doesn't tell you what's happening in your arteries.

The goal isn't to scare you off your diet, your statin, or your clinician's advice. The goal is to make sure your cardiovascular prevention plan is based on what's actually happening in your body, not just on a number that may not tell the whole story. The people counting on you, your wife, your grandkids, your community, deserve the complete picture.

Frequently Asked Questions

Quick answers to the questions that come up most often around this topic.

Does high LDL on keto mean I'm building plaque?

Not necessarily. The KetoCTA trial found no association between LDL levels and plaque progression in metabolically healthy people on ketogenic diets, even at LDL levels above 250, 350, and 450 mg/dL. Some participants with sky-high LDL actually showed plaque regression. The only way to know what's happening in your arteries is to image them directly with CT angiography or coronary calcium scoring. Don't assume danger from a number alone.

Is ApoB a better predictor of plaque growth than LDL?

In this study, no. All four analyses found no association between ApoB and plaque progression. ApoB is part of the causal pathway of atherosclerosis broadly, but in metabolically healthy ketogenic dieters, it didn't predict who built more plaque. The strongest predictor was existing plaque burden at baseline. Plaque begets plaque.

My doctor says my LDL is dangerously high on keto. Should I be worried?

The honest answer: maybe, maybe not. A high LDL number alone doesn't tell you whether plaque is actually building. What tells you is direct imaging, a CT angiogram or coronary calcium score. If you're metabolically healthy, your inflammatory markers are low, and your arteries are clean on imaging, the number may not carry the risk your doctor assumes. Ask for the test that answers the actual question.

What actually predicts plaque growth if not LDL?

Baseline plaque burden. Across all four analyses in the KetoCTA trial, the single strongest predictor of future plaque progression was how much plaque was already present at the first scan. People with more plaque at baseline were more likely to have more plaque at follow-up. People with clean arteries at baseline mostly stayed clean, regardless of their LDL level.

Can plaque actually shrink on a ketogenic diet?

Yes, in some people. The KetoCTA trial confirmed plaque regression in a subset of participants with very high LDL. This was verified by three of the four analyses (semi-quantitative, HeartFlow, and Qangio). Regression isn't guaranteed, and some participants progressed rapidly, but the existence of regression in people with sky-high LDL challenges the simple "high LDL equals growing plaque" narrative.

Is the KetoCTA study reliable given the controversy?

The core findings are robust. Four independent analyses using different methodologies and different teams all agree: LDL and ApoB do not associate with plaque progression in this cohort. Three of the four broadly agree on the magnitude of progression. One (Cleerly) disagrees on magnitude, shows no regressors, and has unresolved quality-control concerns. The study's redundancy, four reads instead of one, actually makes it more rigorous than most.

Should I stop taking my statin based on this study?

No. Do not change your medication based on one study or one article. This trial enrolled metabolically healthy lean mass hyper-responders on ketogenic diets. It does not apply to everyone with high LDL. If you have existing plaque, metabolic disease, or other risk factors, a statin may still be the right call. What this study does support is asking your clinician for direct imaging to know your actual plaque status, so treatment decisions are based on what's really happening.

What testing should I ask for if my LDL is high on keto?

Start with direct imaging: a coronary calcium score (CAC) at minimum, and ideally a CT angiogram (CTA) for the most complete picture of soft and calcified plaque. Add metabolic testing: OGTT/IR for insulin response, hsCRP for inflammation, ApoB for particle count in context, and lipid fractionation. These tests tell you whether your elevated LDL is translating into actual arterial disease or whether your metabolic health is protecting you.

How PrevMed Helps

If your LDL went up on keto and your doctor is pushing a statin based on the number alone, without ever imaging your arteries, you're right to want a better answer.

The standard annual physical wasn't built to answer the question that actually matters: is plaque growing in my arteries right now? It was built to treat numbers. And as this study shows, numbers alone may not tell you what's happening inside. The PrevMed testing protocol gives you the direct answer: CT angiography for plaque visualization, OGTT/IR for insulin response, hsCRP for inflammation, and lipid fractionation with ApoB in clinical context.

To find out where you actually stand, take the PrevMed Heart Attack Prevention Assessment. The people counting on you deserve an answer based on evidence, not assumption.

*Educational disclaimer: This article is for educational purposes only and does not constitute medical advice. Consult your physician before making changes to your diet, medication, or testing plan, particularly if you have an existing cardiovascular or metabolic condition. Do not stop or modify any prescription without speaking to your prescriber.*

References

  • Feldman D, Budoff MJ, Soto AE. Plaque Begets Plaque. ApoB Does Not: Results from the KetoCTA Trial. Published April 2025. [DOI pending — confirm with research team]
  • Budoff MJ, et al. Assessment of coronary artery disease by cardiac computed tomography: a scientific statement from the American Heart Association. Circulation. 2006;114(16):1761-1791. DOI: 10.1161/CIRCULATIONAHA.106.178458
  • Ridker PM, et al. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med. 2000;342(12):836-843. DOI: 10.1056/NEJM200003233421202
  • Reaven GM. Insulin resistance: the link between obesity and cardiovascular disease. Med Clin North Am. 2011;95(5):875-892. DOI: 10.1016/j.mcna.2011.06.002

Additional reading

This article is for educational purposes and isn’t medical advice. Talk to a clinician about decisions specific to your health.