Longitudinal Data From the KETO-CTA Study: Plaque Predicts Plaque, ApoB Does Not.
Level 3 - non-randomized controlled study
Prospective longitudinal observational cohort study without a randomized control group
PubMed 40192608 · doi:10.1016/j.jacadv.2025.101686
What was done
A total of 100 individuals on a ketogenic diet with diet-induced LDL-C ≥190 mg/dL, HDL-C ≥60 mg/dL, and triglycerides ≤80 mg/dL were followed prospectively for 1 year. Plaque progression was assessed using coronary artery calcium (CAC) scoring and coronary computed tomography angiography (CCTA). Linear regression and Bayes factors were used to evaluate predictors of progression alongside sensitivity analyses for diet adherence and baseline cardiovascular risk.
What was found
At baseline, participants had a median ApoB of 178 mg/dL (Q1-Q3: 149-214 mg/dL), LDL-C of 237 mg/dL (Q1-Q3: 202-308 mg/dL), and total plaque score (TPS) of 0 (Q1-Q3: 0-2.25). Over 1 year, median change in noncalcified plaque volume (NCPV) was 18.9 mm³ (IQR: 9.3-47.0 mm³) and percent atheroma volume (PAV) increased by a median of 0.8% (IQR: 0.3%-1.7%). Baseline ApoB, change in ApoB (median change 3 mg/dL, Q1-Q3: -17 to 35 mg/dL), and total LDL-C exposure (median 1,302 days, Q1-Q3: 984-1,754 days) were not associated with changes in NCPV or TPS. Bayes factors supported the null hypothesis of no ApoB association by 6- to 10-fold. All baseline plaque metrics (CAC, NCPV, TPS, and PAV) strongly predicted change in NCPV.
Why it matters
The study suggests that among lean individuals with ketogenic diet-induced hypercholesterolemia, existing baseline plaque burden rather than short-term ApoB or LDL-C exposure predicts 1-year anatomical plaque progression.
Limits
The study had a small sample size (n=100), lacked a normolipidemic control group, evaluated only surrogate imaging markers over a short 1-year follow-up, and is indexed as a retracted publication.
Cited by
- supports A published 100-person study by Dave Feldman showed that arterial plaque progression or regression in lean mass hyper-responders was not related to LDL or ApoB levels.