Low Carb High Fat - Ketogenic

78 readers

8 users here now

A casual community to talk about LCHF/Ketogenic lifestyles, issues, benefits, difficulties, recipes, foods.

The more science focused sister community is [email protected]

Rules

Be nice
Stay on topic
Don’t farm rage
Be respectful of other diets, choices, lifestyles!!!
No Blanket down voting - If you only come to this community to downvote its the wrong community for you

founded 3 months ago

MODERATORS

[email protected]

Paper - Plaque Begets Plaque, ApoB Does Not: Longitudinal Data From the KETO-CTA Trial - 2025 (hackertalks.com)

submitted 6 days ago* (last edited 6 days ago) by [email protected] to c/[email protected]

3 comments fedilink hide all child comments

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

you are viewing a single comment's thread
view the rest of the comments

[–] [email protected] 2 points 6 days ago* (last edited 6 days 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