Uploaded August 2025 | Updated September 2026, 19 minutes ago
NOTE: this Q&A session followed Dave's presentation on preliminary data for Keto-CTA following all four analyses now in hand -- you can watch it here: youtube.com/watch?v=aJobOSRdIOM
In this Q&A session, Dave Feldman addresses audience questions about the Keto-CTA study, including participant adherence, cardiovascular risk in Lean Mass Hyper-Responders (LMHRs), imaging variability, plaque regression, and quality control protocols. He discusses insights from multiple imaging analyses, emphasizes the importance of personalized risk assessment, and explains why rigorous blinding and longer-term follow-ups are essential for interpreting results.
0:01 — Did the Citizen Science Foundation pay Cleerly for their analysis?
An audience member asked whether CSF funded Cleerly’s imaging work. Dave clarified that the foundation funded the study itself through Lundquist and offered to fully pay for a blinded quality control (QC) review. Payment was not a limiting factor.
0:40 — How was dietary adherence ensured?
Dave explained that Keto-Mojo provided glucose and ketone meters for all 100 participants, enabling continuous adherence tracking throughout the year.
1:30 — Does the study prove LMHRs are high- or low-risk?
An audience member asked whether the findings show LMHRs are inherently high-risk. Dave emphasized that neither extreme applies: as a group, LMHRs are not defined as high-risk, though some participants showed progression. Imaging highlights significant individual variability.
3:36 — The role of imaging in risk assessment
Dave stressed that imaging, particularly CAC scoring, remains a powerful risk-prediction tool. However, plaque analysis technologies are still developing and can produce variability across repeated scans.
5:20 — Why do some develop atherosclerosis while others don’t?
From the waterfall plots, the data showed both regression and progression but no clear association with LDL-C or ApoB. Dave agreed this underscores that, at a population level, we still cannot reliably predict who develops disease — supporting the value of personalized, imaging-driven care.
6:07 — Where does functional testing fit in?
One question raised concerns about overtreatment based solely on imaging. Dave acknowledged the risk but stressed that well-conducted randomized controlled trials remain critical for guiding care.
7:03 — Lowering LDL/ApoB despite no observed association
An audience member asked whether lowering LDL or ApoB could still benefit those with higher plaque burden despite no association in this study. Dave said it’s plausible but unproven, requiring a separate, targeted study.
10:01 — Variability in plaque regression signals
Dave cautioned that small regression changes may fall within imaging noise and highlighted the importance of a third scan at 4–5 years to better confirm true trajectories.
12:07 — How reliable is a CAC score of zero?
While a CAC score of zero is highly prognostic, Dave noted it’s not absolute — rare cases involve non-calcified plaque or occlusions.
13:02 — Was exercise frequency tracked?
Dave confirmed exercise patterns weren’t tracked but expressed concern that over-exercisers within the LMHR group might impact vascular health if recovery isn’t prioritized.
14:18 — Vitamin K2 and calcification changes
Asked about calcification shifts, Dave confirmed changes occurred in both directions but highlighted discrepancies in the Cleerly dataset, favoring corroborated results from other analyses.
15:38 — Understanding what drives plaque regression
Dave confirmed that sub-analyses are planned but emphasized that three-scan trajectories will be needed to distinguish true biological change from measurement variability.
17:11 — Imaging variability and AI vs. human reads
Dave explained that contrast timing, scanner settings, and algorithms all introduce variability, making rigorous blinding and standardized protocols essential.
19:44 — Quality control and double-blinding protocols
Dave revealed that metadata errors compromised full blinding in initial Cleerly reads, which is why a fully blinded QC pass remains a priority.
22:03 — Are Cleerly’s imaging methods reliable?
Asked if Cleerly’s technology is flawed, Dave clarified he doesn't assume there's inherent issues with the technology. The discrepancies may simply relate to this specific dataset, underscoring the need for independent validation.
NOTE: this Q&A session followed Dave's presentation on preliminary data for Keto-CTA following all four analyses now in hand -- you can watch it here: youtube.com/watch?v=aJobOSRdIOM
In this Q&A session, Dave Feldman addresses audience questions about the Keto-CTA study, including participant adherence, cardiovascular risk in Lean Mass Hyper-Responders (LMHRs), imaging variability, plaque regression, and quality control protocols. He discusses insights from multiple imaging analyses, emphasizes the importance of personalized risk assessment, and explains why rigorous blinding and longer-term follow-ups are essential for interpreting results.
0:01 — Did the Citizen Science Foundation pay Cleerly for their analysis?
An audience member asked whether CSF funded Cleerly’s imaging work. Dave clarified that the foundation funded the study itself through Lundquist and offered to fully pay for a blinded quality control (QC) review. Payment was not a limiting factor.
0:40 — How was dietary adherence ensured?
Dave explained that Keto-Mojo provided glucose and ketone meters for all 100 participants, enabling continuous adherence tracking throughout the year.
1:30 — Does the study prove LMHRs are high- or low-risk?
An audience member asked whether the findings show LMHRs are inherently high-risk. Dave emphasized that neither extreme applies: as a group, LMHRs are not defined as high-risk, though some participants showed progression. Imaging highlights significant individual variability.
3:36 — The role of imaging in risk assessment
Dave stressed that imaging, particularly CAC scoring, remains a powerful risk-prediction tool. However, plaque analysis technologies are still developing and can produce variability across repeated scans.
5:20 — Why do some develop atherosclerosis while others don’t?
From the waterfall plots, the data showed both regression and progression but no clear association with LDL-C or ApoB. Dave agreed this underscores that, at a population level, we still cannot reliably predict who develops disease — supporting the value of personalized, imaging-driven care.
6:07 — Where does functional testing fit in?
One question raised concerns about overtreatment based solely on imaging. Dave acknowledged the risk but stressed that well-conducted randomized controlled trials remain critical for guiding care.
7:03 — Lowering LDL/ApoB despite no observed association
An audience member asked whether lowering LDL or ApoB could still benefit those with higher plaque burden despite no association in this study. Dave said it’s plausible but unproven, requiring a separate, targeted study.
10:01 — Variability in plaque regression signals
Dave cautioned that small regression changes may fall within imaging noise and highlighted the importance of a third scan at 4–5 years to better confirm true trajectories.
12:07 — How reliable is a CAC score of zero?
While a CAC score of zero is highly prognostic, Dave noted it’s not absolute — rare cases involve non-calcified plaque or occlusions.
13:02 — Was exercise frequency tracked?
Dave confirmed exercise patterns weren’t tracked but expressed concern that over-exercisers within the LMHR group might impact vascular health if recovery isn’t prioritized.
14:18 — Vitamin K2 and calcification changes
Asked about calcification shifts, Dave confirmed changes occurred in both directions but highlighted discrepancies in the Cleerly dataset, favoring corroborated results from other analyses.
15:38 — Understanding what drives plaque regression
Dave confirmed that sub-analyses are planned but emphasized that three-scan trajectories will be needed to distinguish true biological change from measurement variability.
17:11 — Imaging variability and AI vs. human reads
Dave explained that contrast timing, scanner settings, and algorithms all introduce variability, making rigorous blinding and standardized protocols essential.
19:44 — Quality control and double-blinding protocols
Dave revealed that metadata errors compromised full blinding in initial Cleerly reads, which is why a fully blinded QC pass remains a priority.
22:03 — Are Cleerly’s imaging methods reliable?
Asked if Cleerly’s technology is flawed, Dave clarified he doesn't assume there's inherent issues with the technology. The discrepancies may simply relate to this specific dataset, underscoring the need for independent validation.

![BREAKING – New Analysis of Heart Scan Data (CCTA) for Extremely high LDL vs Average LDL Cholesterol
BREAKING: Dr Matt Budoff has now presented the matched analysis for:
KETO (#LMHRstudy) vs Control (#MiHeart)
METHODS – 80 Participants of #LMHRstudy fell within #MiHeart age range and were then matched 1:1 for age, gender, race, diabetes mellitus, hyperlipidemia, hypertension, and past smoking to asymptomatic subjects from the #MiHeart cohort.
PRIMARY ANALYSIS – High resolution heart scans (#CCTA) allowing for primary analysis of Total Plaque Score (TPS), Total Stenosis Score (TSS) and Segment Involvement Score (SIS)
RESULTS
The matched mean age was 55.5 years, with mean #LDL cholesterol of 272 mg/dL (max LDL-C 591) mg/dl and mean 4.7 years duration on a ketogenic diet.
🚨 There was no significant difference in coronary plaque burden of #LMHRstudy (mean LDL-C 272) cohort as compared to #MiHeart controls (mean LDL 123 mg/dl); nb: pre-KETO LDL-C in KETO group was 122 mg/dl
🚨 There was no significant difference in CAC (median and IQR) [0 (0,56)] versus [1 (0, 49)], p = 0.520
🚨 No relationship of LDL-C elevations and plaque
⚠️ is still ongoing for second CCTA completion in our cohort by February of 2024. And as always, please continue to work with your doctor.
- I will have my own video reaction and thoughts in the coming hours.
🙏🙏🙏 to everyone and I mean everyone who helped us get to this pivotal milestone. 🙏🙏🙏 BREAKING – New Analysis of Heart Scan Data (CCTA) for Extremely high LDL vs Average LDL Cholesterol](https://i.ytimg.com/vi/ny2JqAgoORo/mqdefault.jpg)





![#CholesterolScience – with Ethan Weiss, MD
Hosted by Dave Feldman :: Produced by Siobhan Huggins
0:00 Intro and Ethan’s background
3:33 Cholesterol Skeptics and Concerned Medical Professionals – meeting in the middle.
( https://cholesterolcode.com/wp-content/uploads/2019/08/CholesterolScience-with-Ethan-Weiss.png )
8:20 How many patients does Ethan feel reach a decent level of knowledge about lipidology and cardiology?
10:15 Navigating the discussion on the benefits/risks of lipid changes from diet
17:15 When cholesterol is elevated for a metabolic reason alone – does it pose a greater risk?
( https://cholesterolcode.com/wp-content/uploads/2019/08/CholesterolScience-with-Ethan-Weiss-1.png )
( https://cholesterolcode.com/wp-content/uploads/2019/08/key-question.png )
23:00 Giving doctors the benefit of the doubt – are doctors just trying to help?
27:10 Dave’s disappointment with perceived lack of curiosity from the medicalsphere.
30:15 The difficulty in discussing possible benefits from lipoproteins and potential influence on all-cause mortality
36:50 Nuances of data collection and statin trials
- Study mentioned: MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20 536 high-risk individuals: a randomised placebo controlled trial https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(02)09327-3/fulltext
Note from producer:
In the efficacy and safety statement for the trial mentioned it lists Merck Sharp & Dohme (manufacturers of simvastatin) as well as Hoffmann-La Roche (manufacturers of the vitamins used) as providing partial funding for the study:
The study is being funded by the UK Medical Research Council, the British Heart Foundation, Merck Sharp & Dohme (manufacturers of simvastatin[…]) and Hoffmann-La Roche (manufacturers of the vitamins[…]) https://doi.org/10.1053/euhj.1998.1350
- However in the published paper of the results it states the following:
The Clinical Trial Service Unit has a staff policy of not accepting honoraria or other payments from the pharmaceutical industry, except for the reimbursement of costs to participate in scientific meetings. https://doi.org/10.1016/S0140-6736(02)09327-3
44:56 If there were a trial that showed that people with high HDL, high LDL, and low triglycerides didn’t benefit from statins would [Ethan] want to know that information? (https://twitter.com/erreyedoc/status/1162070100037574656)
- Study mentioned: Influence of Low High-Density Lipoprotein Cholesterol and Elevated Triglyceride on Coronary Heart Disease Events and Response to Simvastatin Therapy in 4S https://www.ahajournals.org/doi/full/10.1161/hc5001.100624
52:40 Open data, machine learning, and possibilities moving forward
56:20 Non-HDL and mortality from the NHANES dataset
https://twitter.com/DaveKeto/status/1133177415486693376?s=20
58:30 Changes in ability to connect with researchers and scientists
1:00:05 What does Dave mean by risk?
1:04:10 Modifications to low carb to achieve lower LDL
1:08:55 What Dave has learned about the importance of rigorousness in self-experimentation
1:13:29 Can self-experiments have benefits applicable to people beyond the person doing them?
1:17:29 Cholesterol biosynthesis
1:18:40 Reverse causality – is there a possibility that the lipoproteins are reflecting a problem and not causing it?
Note from producer: I attempted a follow-up to see if I could find any studies looking at the impact of infusion of native mouse lipoproteins on atherosclerosis development, but I have not found any thus far.
1:24:33 Clotting, vascular injury, and engineering
1:29:55 The impact of placebo
Podcast mentioned: The Hidden Brain: The Untapped Potential of Placebos to Heal (transcript available) https://www.npr.org/2019/04/29/718227789/all-the-worlds-a-stage-including-the-doctor-s-office
1:33:23 The impact of seeing lipids change – could this impact the results of the study?
1:35:56 If it were dose dependency would all drugs that lower LDL have a likewise decrease in cardiovascular disease mortality?
1:38:46 Drug trials – ideals, replication, and funding
1:42:35 Wrap up and outro
Ethan Weiss Contact:
Twitter: @ethanjweiss #CholesterolScience – with Ethan Weiss, MD](https://i.ytimg.com/vi/phfHRZ_aME8/mqdefault.jpg)


