this post was submitted on 07 Apr 2025
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Paper - Plaque Begets Plaque, ApoB Does Not: Longitudinal Data From the KETO-CTA Trial - 2025 (hackertalks.com)
submitted 2 weeks ago* (last edited 2 weeks ago) by [email protected] to c/[email protected]
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TLDR - If you are a ketogenic lean mass hyper responder with high LDL, insist on imaging to determine your atherosclerotic risk, as this study indicates the LDL and ApoB by itself doesn't indicate a growth in plaque.

Background - Changes in low-density lipoprotein cholesterol (LDL-C) among people following a ketogenic diet (KD) are heterogeneous. Prior work has identified an inverse association between body mass index and change in LDL-C. However, the cardiovascular disease risk implications of these lipid changes remain unknown.

Objectives - The aim of the study was to examine the association between plaque progression and its predicting factors.

Methods - One hundred individuals exhibiting KD-induced LDL-C ≥190 mg/dL, high-density lipoprotein cholesterol ≥60 mg/dL, and triglycerides ≤80 mg/dL were followed for 1 year using coronary artery calcium and coronary computed tomography angiography. Plaque progression predictors were assessed with linear regression and Bayes factors. Diet adherence and baseline cardiovascular disease risk sensitivity analyses were performed.

Results - High apolipoprotein B (ApoB) (median 178 mg/dL, Q1-Q3: 149-214 mg/dL) and LDL-C (median 237 mg/dL, Q1-Q3: 202-308 mg/dL) with low total plaque score (TPS) (median 0, Q1-Q3: 0-2.25) were observed at baseline. Neither change in ApoB (median 3 mg/dL, Q1-Q3: −17 to 35), baseline ApoB, nor total LDL-C exposure (median 1,302 days, Q1-Q3: 984-1,754 days) were associated with the change in noncalcified plaque volume (NCPV) or TPS. Bayesian inference calculations were between 6 and 10 times more supportive of the null hypothesis (no association between ApoB and plaque progression) than of the alternative hypothesis. All baseline plaque metrics (coronary artery calcium, NCPV, total plaque score, and percent atheroma volume) were strongly associated with the change in NCPV.

Conclusions - In lean metabolically healthy people on KD, neither total exposure nor changes in baseline levels of ApoB and LDL-C were associated with changes in plaque. Conversely, baseline plaque was associated with plaque progression, supporting the notion that, in this population, plaque begets plaque but ApoB does not. (Diet-induced Elevations in LDL-C and Progression of Atherosclerosis [Keto-CTA]

Full Paper: https://doi.org/10.1016/j.jacadv.2025.101686

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[–] [email protected] 1 points 1 day ago* (last edited 1 day ago)

Dave Feldman does a interview going over the controversy of the Keto-CTA study https://youtu.be/xP0jK39yHds

Dave Feldman summerizer

Discussing Keto-CTA with Darius Sharpe

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In this interview with Darius Sharpe, Dave Feldman addresses criticism regarding the recent Keto-CTA study, especially focusing on the oversight of not including crucial numerical data in the results. He acknowledges mistakes made during the publication and emphasizes the importance of transparency and communication with their audience. The discussion revolves around the findings related to LDL levels, plaque progression, and the need for better reporting in future studies, as well as the view that further research is required to understand the implications of these results.

Key Points

Error in Data Presentation

Dave Feldman admits to a significant oversight in the Keto-CTA study, where the primary endpoint numerical data was not included in the publication, which led to considerable frustration among supporters and critics alike. He takes personal responsibility for this mistake and highlights the need for better communication and transparency.

Community Frustration

Darius Sharpe expresses concerns from the community regarding the lack of accessible data after the study's publication, emphasizing that supporters expected concrete results that were not delivered. This sentiment is echoed by many who have invested time and money into the study, demanding accountability and clarity.

Clarification of Study Findings

Dave explains that the Keto-CTA study demonstrated a lack of association between high LDL levels and plaque progression, but acknowledged that the significant increase in plaque volume over the year raised questions that need further investigation. He outlines the heterogeneous nature of the data and the need for careful analysis moving forward.

Planned Future Research

Both speakers discuss the importance of future studies to explore the data collected during the Keto-CTA study, suggesting that more papers will be written to shed light on various aspects of the data. The aim is to use this research to better understand the relationship between diet, LDL levels, and cardiovascular health.

Emphasis on Individualized Care

The conversation concludes with a focus on the importance of individual health metrics, encouraging listeners to seek appropriate imaging to assess their cardiovascular health and adjust their diets accordingly. The idea is to ensure each person's unique health journey is considered in managing their dietary and health choices.

Stephen Thomas also does a paper review https://youtu.be/auXq5jQs0aY

stephen thomas summerizer

Keto CTA Study and More

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In this video, Coach Stephen discusses a recent keto study focusing on the impact of LDL levels on coronary plaque in lean mass hyper-responders. He critiques the study methodology, highlights historical biases in cholesterol research, and emphasizes the need for better data interpretation and control groups. Stephen also addresses the confusion surrounding HbA1c levels and their implications for individuals on a carnivore or keto diet.

Key Points

Historical issues with cholesterol research

Stephen explains the origins of cholesterol studies, beginning with a dubious experiment in the 1910s where rabbits were fed cholesterol to observe plaque formation. He critiques how these early studies laid a flawed foundation for the belief that LDL cholesterol directly causes heart disease.

Flaws in the National Cholesterol Education Program

He describes how the National Cholesterol Education Program, starting in the late 1980s, correlated with increased statin prescriptions and emphasized LDL levels as a guiding metric for health, showing conflicts of interest in the members involved.

Limitations of the recent keto study

The recent study on lean mass hyper-responders is critiqued for its lack of control groups and the implications of self-reported dietary adherence. Stephen argues that without randomization, the data may not reliably reflect broader population impacts.

Critique of ApoB and LDL theories

Stephen notes that the correlation between increasing ApoB levels and plaque progression is not substantiated by the study's data, suggesting that high LDL levels do not inherently lead to heart disease.

Discussion on HbA1c levels in ketogenic diets

He discusses the rise in HbA1c levels in individuals on a ketogenic diet, explaining that these levels can be misleading due to factors such as the lifespan of red blood cells, emphasizing a need for further investigation into blood glucose metrics for those on high-fat diets.

[–] [email protected] 1 points 6 days ago* (last edited 6 days ago)

Bart Kay (PhD) has a response to the paper https://youtu.be/MtIhLnxqNrQ?t=2520

He is not a happy camper, he does not like Norwitz.

  • Lacks wisdom and experience of a senior scientist, which is needed to attack an entrenched dogma
  • Given the anti-keto crowd ammunition, to attack keto by virtue of weak science
  • This paper does not help
  • The staff are not unassailable
  • The paper is a waste of time, and counter productive
  • This paper is incapable of inferring on cause and effect, so the title is wrong "plaque begets plaque" which implies causation
  • very delimited population, not a random sample, no control exerted - cannot inform on cause or effect
  • Primary outcome measure: soft plaque on arteries... primary outcome isn't clearly indicated in the paper. its bad optics to not bring the primary outcome measure

etc, etc... but its a vicious and through teardown.

[–] [email protected] 2 points 2 weeks ago* (last edited 2 weeks ago)

Notes from the paper:

All participants were asked to stay on a KD during their follow-up, and to measure adherence, 3 dietary recalls and daily b-hydroxybutyrate (bHB) data were collected using the Automated Self-Administered 24-Hour (ASA24) Dietary Assessment Tool from the National Institutes of Health. Blood bHB monitoring devices by KetoMojo (Napa) were provided to each participant.

Look at that, they verified ketone state!

with 87% of the cohort recording values above >=0.3 mmol/L on a majority of measurements, a threshold chosen given the known steady-state drop in circulating ketone levels with prolonged adaptation

However, this does not mean that the LMHR population is without risk. The observed, the observed PAV progression in this KETO-CTA cohort was comparable to what has been observed in other studies on populations with lower LDL-C across the cardiovascular disease risk spectrum. It should be emphasized that this includes heterogeneity in progression (and regression) across the population

despite profound elevations in LDL-C and ApoB, based on these data, LMHR subjects with CAC 0 at baseline (n 57) constitute a low-risk group for PAV progression, even as compared to other cohorts with far lower LDL-C and ApoB. By contrast, LMHR subjects with elevated baseline CAC, possibly from a history of metabolic damage and dysfunction prior to adopting a CRD, appear to constitute a relatively higher risk group for PAV progression even where LDL-C and ApoB are equal to their CAC counterparts.

the dropout rate was 0%, and adherence to the KD was assessed by dietary records and bHB measurements

For these 100 people the KD was sustainable

[–] [email protected] 2 points 2 weeks ago* (last edited 2 weeks ago)

Nick Norwitz (author) does a great video presentation of this: https://youtu.be/a_ROZPW9WrY

If you prefer a written summary: https://staycuriousmetabolism.substack.com/p/big-news-the-lean-mass-hyper-responder

100 people, prospective study, with plaque imaging, a very strong signal.

TLDR: the Lean Mass Hyper Responders (LMHR) following a ketogenic diet with high LDL do not show a growth in plaque over the period of 1 year. 6 people showed a reduction in plaque.

  • Most participants showed no or minimal progression of coronary plaque

  • Neither ApoB nor LDL exposure predicted plaque progression

While both LDL-C and ApoB are independent risk factors for atherosclerosis, the absolute risk associated with elevated LDL-C and ApoB is CONTEXT-DEPENDENT, including the etiology (cause) of the elevations in these biomarkers, LDL-C and ApoB as well as interactions with other risk markers, like insulin resistance

high LDL-C and ApoB among a metabolically healthy population have different cardiovascular risk implications than high LDL-C among those with metabolic dysfunction.

  • Elevations in LDL-C and ApoB are dynamic and result from a metabolic response to carbohydrate restriction, rather than as a function of a genetic defect. These people aren’t born with high LDL, it’s a response to carbohydrate restriction having to do with energy flux through the body.

  • These participants are of normal-health weight (BMI <25 kg/m2) and metabolically healthy rather than living with obesity, pre-diabetes or type 2 diabetes or other insulin resistance disorders.

  • The high LDL-C and ApoB in this phenotype emerge as part of a lipid triad, also inclusive of high HDL-C and low triglycerides, representing a metabolic signature of a distinct physiological state.

[–] [email protected] 1 points 2 weeks ago* (last edited 2 weeks ago)

Dr Aseem Malhorta a cardiologist does a great interview on the paper with Nick Norwitz https://youtu.be/I9TOMH332eA

Dr. Scher and Dave Feldman do a detailed 45m paper review https://www.youtube.com/watch?v=UzyAVqPaSrk

Dr. Scher and Dr. Budoff have a 20m talk about the study https://www.youtube.com/watch?v=HfCFljZ4i6w

Dr. Brewer and Dave Feldman do a hour long interview https://youtu.be/wGaY4-v1gI0

Dave Feldman (author) did a tiny presentation: https://youtu.be/HJJGHQDE_uM

Dr Scher also covers it https://www.youtube.com/watch?v=RSGj6UJusTg

Dr Berry also covers it https://youtu.be/qpn5g-v26K4