High LDL on Keto and Heart Plaque, What This Study Found

What most people get wrong about LDL and plaque

A lot of cholesterol conversations start with a single assumption: if LDL cholesterol is high, plaque must be building in the heart.

This video pushes back on that simplification, not by claiming LDL is irrelevant, but by spotlighting a group of people who break the usual pattern.

The discussion centers on a recently published study led by Nicholas Norwitz and colleagues, including David Feldman and Matthew Budoff, looking at people on long-term carbohydrate restriction who develop strikingly high LDL levels. These individuals are often metabolically healthy, lean, and physically active, which makes them a fascinating stress test of the usual “high LDL equals high plaque” narrative.

At the same time, the video is careful about one point that matters: the study is not a randomized controlled trial. It is an observational comparison of two cohorts that were matched across several health characteristics.

That distinction is not a footnote. It is the difference between “this pattern is interesting” and “this proves cause and effect.”

Important: A single study that finds no association in one population does not erase decades of evidence linking ApoB-containing lipoproteins (including LDL) with atherosclerotic cardiovascular disease. It does, however, raise a practical question: Are there contexts where very high LDL does not track with plaque burden, at least over a certain time horizon?

The study being discussed, the KETO Trial in plain language

The paper highlighted in the video is titled “Carbohydrate restriction-induced elevations in LDL cholesterol and atherosclerosis: the KETO Trial.” The central comparison is straightforward.

Matching matters because it attempts to make the groups comparable on major cardiovascular risk factors. In the video, the matched variables include age, sex, race, diabetes status, high blood pressure, and past smoking status.

The core question was whether the keto group, despite having LDL levels that were dramatically higher, had more coronary plaque on advanced imaging.

What the research shows

What the research shows: In this matched comparison, the keto lean mass hyperresponders had markedly higher LDL cholesterol but did not have a greater coronary plaque burden on coronary CT angiography compared with controls.

The study itself can be found in the scientific literature, and the imaging approach used here aligns with how cardiology often evaluates coronary atherosclerosis risk in practice, especially when looking beyond basic cholesterol panels.

For background on coronary calcium scoring as a risk tool, see the American Heart Association overview of coronary artery calcium tests hereTrusted Source.

Who are lean mass hyperresponders, and why their labs look unusual

Lean mass hyperresponders are not just “people with high LDL.” The phenotype is typically described as a combination of:

This pattern tends to show up after carbohydrate restriction, particularly in people who are relatively lean and metabolically healthy.

The video also notes an important exclusion: participants were not identified as having familial hypercholesterolemia in this cohort. That matters because genetically driven lifelong LDL elevation is a different scenario than diet-associated changes, even if the LDL number looks similar.

Another nuance emphasized is that LDL can rise for many reasons, not only keto. The video points out that diets high in refined foods and sugar can also raise cholesterol in some people.

That is a key trade-off in real life: people often compare “keto LDL” to an idealized low-LDL scenario, when the alternative for many people is not a perfect Mediterranean pattern, it is muffins, pastries, and sugar-heavy processed foods.

Did you know? LDL is only one piece of the risk puzzle. Many cardiology risk models also weigh blood pressure, diabetes, smoking, and age heavily, because these factors strongly predict events at the population level. The CDC summarizes major heart disease risk factors hereTrusted Source.

What the heart scans measured, CAC, CCTA, and plaque scores

A major strength of the study discussed is that it did not rely only on blood tests. It used imaging.

The video focuses on CCTA, short for coronary computed tomography angiography (a CT-based method that visualizes coronary arteries and can characterize plaque). It also discusses coronary artery calcium (CAC) scoring, which quantifies calcified plaque.

These tools are related but not identical.

This matters because a person can have a CAC score of zero and still have non-calcified plaque, especially at younger ages. Conversely, calcification can also represent more stable plaque in some contexts.

For a deeper explanation of what a CAC score means and how it is used clinically, the American College of Cardiology has patient-facing and clinician-facing resources, and the concept is summarized in many cardiology prevention discussions. A practical overview is also described by the AHA hereTrusted Source.

The headline finding, very high LDL was not linked to more plaque here

Here is the striking comparison highlighted repeatedly in the video.

In the keto lean mass hyperresponder group, LDL cholesterol was more than double that of the matched Miami Heart controls. Triglycerides were much lower, and HDL was about one-and-a-half times higher.

Yet, when coronary plaque burden was compared, there were no significant differences in measures like CAC, stenosis, and total plaque scoring.

The video also describes the distribution in a very human way: there were outliers in both groups. One keto participant had a high plaque score, and there were also high-score outliers in the Miami Heart controls. The median plaque levels were similar.

That detail is important because it discourages a simplistic interpretation like “keto prevents plaque” or “LDL never matters.” Real datasets almost always contain heterogeneity.

This is where the study’s unique perspective lands: in a metabolically healthy cohort with carbohydrate restriction-associated LDL elevation over an average of about 4.7 years, plaque burden was not higher than in matched controls with much lower LDL.

Expert Q&A box

Q: Does this mean high LDL is harmless if you are metabolically healthy?

A: Not necessarily. This study suggests that in this specific phenotype and timeframe, very high LDL was not associated with higher plaque burden on CCTA compared with matched controls. But because it is not randomized, it cannot prove that high LDL is safe for everyone or over longer periods.

A reasonable takeaway is that risk assessment may need more context than LDL alone, including metabolic health, blood pressure, smoking history, and sometimes imaging. If you have very high LDL, it is worth discussing a personalized plan with a clinician.

Health Writer, medically cautious summary of the study discussed in the video

A key idea from the video, LDL may be necessary but insufficient

The video repeatedly returns to a mechanistic framing: LDL is part of the atherosclerosis story, but it may not be the entire story.

The phrasing used is essentially: LDL may be necessary but insufficient.

This framing emphasizes steps like LDL entering the artery wall, becoming modified or oxidized, being taken up by macrophages, forming foam cells, and eventually contributing to plaque and calcification.

Oxidative stress and endothelial injury become key supporting actors in this narrative.

The discussion highlights several factors that may increase the chance that LDL becomes “problematic” in the artery wall:

This is broadly consistent with mainstream cardiovascular prevention frameworks that focus heavily on blood pressure, diabetes, and smoking cessation, even while still treating LDL and ApoB as causal risk factors.

For a mainstream consensus view on LDL and atherosclerotic risk, the American Heart Association discusses cholesterol and cardiovascular risk factors hereTrusted Source.

Still, the unique angle in the video is the emphasis on context: LDL may be more dangerous when paired with metabolic dysfunction and oxidative stress.

Pro Tip: If you are tracking lipids on a low-carb diet, do not look at LDL in isolation. Consider pairing labs with blood pressure trends, fasting glucose or A1c, and a clinician-guided discussion of whether imaging like CAC or CCTA fits your situation.

Risk context the video keeps returning to, metabolic health

A major theme is that metabolic health may modulate cardiovascular risk.

That shows up in multiple ways.

First, the study participants in the keto cohort were described as metabolically healthy, and the groups were matched for diabetes status. Hemoglobin A1c was not significantly different between groups.

Second, the Q and A portion of the video repeatedly points toward insulin resistance as an important contributor to plaque risk. That does not mean insulin resistance is the only driver, but it is part of a cluster that includes high triglycerides, low HDL, hypertension, and elevated glucose.

Third, the practical advice is heavily lifestyle-focused. The video emphasizes movement, particularly walking after meals, and reducing refined carbohydrates to lower triglycerides.

A single workout can change glucose handling in real time.

The video mentions that a short session on a spin bike can drop blood glucose significantly, and it stresses that skeletal muscle is a major site of insulin action. This is consistent with exercise physiology: muscle contractions increase glucose uptake, and regular activity improves insulin sensitivity.

For a research-backed overview of exercise and cardiometabolic health, see the CDC’s physical activity resources hereTrusted Source.

The triglyceride point, explained simply

The triglyceride advice in the video is blunt: if triglycerides are high, start by cutting refined carbohydrates.

That aligns with common clinical guidance that high triglycerides often reflect excess carbohydrate intake, insulin resistance, alcohol intake, or a mix of factors. The National Heart, Lung, and Blood Institute discusses triglycerides and heart risk hereTrusted Source.

The video also adds a nuance that is easy to miss: triglycerides can rise from “liquid fat” and fried foods too. In other words, it is not only sugar.

Practical next steps to discuss with a clinician if your LDL is high on keto

If you are on a carbohydrate-restricted diet and your LDL is much higher than expected, this video suggests a more layered approach than panic or denial.

It is not “ignore LDL.” It is “place LDL in context, then decide what to do.”

Below is a practical, clinician-friendly checklist that reflects the video’s priorities while staying medically cautious.

How to think through the situation step by step

»MORE: If you want a simple tracking sheet to bring to appointments, create a one-page “cardiometabolic snapshot” that includes blood pressure averages, A1c, triglycerides, HDL, LDL, ApoB, ApoA1, and any imaging results (CAC or CCTA). Having everything on one page can make conversations more productive.

A note on homocysteine, why the video downplays single readings

A viewer asked about a homocysteine level of 17. The response in the video is that homocysteine testing can be finicky and may not be a great standalone assay because of handling issues (for example, delays in processing and not placing samples on ice).

The practical stance is: do not “freak out” over one value, but if levels are consistently high, discuss possible contributors and whether B vitamins like methylated folate and B12 are appropriate.

For general background on homocysteine and cardiovascular risk discussions, MedlinePlus provides a patient-friendly overview hereTrusted Source.

Expert Q&A box

Q: If LDL is not the only driver, what else might be contributing to plaque?

A: The video’s model emphasizes a combination of factors: LDL particles need to enter the artery wall, then oxidative stress and endothelial injury can increase the chance that LDL becomes modified and retained. High blood pressure, smoking, high glucose, insulin resistance, and sedentary behavior are repeatedly named as contributors.

In practice, this means that a “good LDL number” does not erase risk from uncontrolled blood pressure or diabetes, and a “bad LDL number” may not have the same meaning in every metabolic context. A clinician can help interpret these factors together.

Health Writer, medically cautious summary of the mechanisms discussed

Statins, inflammation, and the “why is heart disease still high?” question

The video also addresses a common frustration: if statins are widely prescribed, why is heart disease still so common?

The discussion points to the concept of number needed to treat (NNT) and suggests that benefits can vary widely by population and context, with stronger evidence in secondary prevention (after a heart attack) than in some primary prevention scenarios.

It also emphasizes that statins have effects beyond LDL lowering, including anti-inflammatory effects, and raises concerns about blocking biochemical pathways like the mevalonate or isoprenoid pathway, which relates to compounds such as CoQ10.

This is a nuanced area. If you are considering or already taking a statin, it is best handled as a personalized risk-benefit discussion with your clinician.

For a mainstream, evidence-based overview of statins, including benefits and side effects, see the American Heart Association’s statin information hereTrusted Source.

Key Takeaways