The following preliminary data from the Keto-CTA / LMHR Study were presented on August 18th at Symposium of Metabolic Health in San Diego.
IMPORTANT – These Data are Preliminary. This has not undergone peer review and preparation for publication, but we’ll likely have more to share this in the coming months.
As always, please continue to work with your doctor. This research is an ongoing effort to inform decision making with care providers, but not to replace it.
Match Analysis Presentation from CoSci
Before reading this article, if you haven’t already, please watch Dr. Matt Budoff’s keynote presentation at CoSci this year on the Keto-CTA / LMHR Study match analysis with the Miami Heart study (MiHeart).
These Data are Presented With Limited Analysis
Consider the following data more a capture-and-report
Quick Review of Total Plaque Score (TPS)
The total plaque score (TPS) utilizes the 15-segment American Heart Association model of the coronary arteries. These 15 segments used in a total plaque score are chosen because they represent areas in the arteries that are more susceptible to plaque formation, due to the mechanical forces that contribute to endothelial dysfunction and inflammation. Each plaque rated with a score of 0 – 3 based on plaque volume. TPS is a summation across the 15 segments, yielding a TPS score range of 0 – 45.
Total Plaque Score (TPS) vs Lipid Metrics
Keto CTA (LMHR Study) vs MiHeart
Spearman correlation of general lipid values vs TPS
| KETO | MI HEART | |||
| r | p | r | p | |
| Total Cholesterol | -0.11 | 0.43 | 0.15 | 0.28 |
| LDL-C | -0.08 | 0.58 | 0.26 | 0.06 |
| HDL-C | -0.2 | 0.15 | -0.22 | 0.11 |
| Triglycerides | -0.01 | 0.96 | 0.14 | 0.3 |
Note from Dave: As I discussed from the SMH presentation, these data are not too surprising given the context. See presentation when it’s released for a more in-depth discussion.
Total Plaque Score (TPS) vs Lipid Particle Counts
Total Low Density Lipoprotein Particles (LDL-P) vs TPS
Keto-CTA Only
R2 0.0015 – No correlation between Total LDL Particles (LDL-P) and Total Plaque Score (TPS)
Note from Dave: This was very exciting to see this born out on our data as it has been long speculated on. I’ve had discussions with Peter Attia, Layne Norton, Howard Luks, and many others speculating on high LDL-P and plaque with LMHR at a population level.
Total Plaque Score (TPS) vs Small Dense LDL Particle (sdLDL-P)
R2 0.001 – No correlation between Small LDL Particles (sdLDL-P) and Total Plaque Score (TPS)
Note from Dave: This was likewise exciting to see with the context of the participants of our study as I had speculated on this outcome as well [ie here, here, here. See the talk when it is released for a deeper dive.
Total Plaque Score (TPS) vs Lp(a) & OxPL-ApoB
Total Plaque Score (TPS) vs Lp(a)
R2 0.007 – No correlation between Lp(a) and Total Plaque Score (TPS)
Note from Dave: I’ve had many great discussions with Sam Tsimikas on this given his unique expertise in this area. Indeed, the relevance if Lp(a) in this context outside other acute phase reactants (ie C-Reactive Protein) does appear to be relevant in here. I’ll be interested in seeing our longitudinal data on this as well for comparison with progression too.
Total Plaque Score (TPS) vs OxPL-ApoB
R2 0.0002 – No correlation between OxPL-ApoB and Total Plaque Score (TPS)
Note from Dave: Happy to see this hypothesis get some testing as well. “I think we’ll have many #LMHRs with higher Lp(a) yet lower than expected oxPL-ApoB given both those levels and their ApoB.” While I haven’t seen the aggregates yet, I suspect this may bear out when we are completing the final paper.
Quantitative Analysis
Quantitative analysis using plaque volume and AI-guided reading is a more objective and detailed method compared to the semi-quantitative approach of total plaque score (TPS). Here’s how they compare directly:
- Measurement Precision: While total plaque score offers a rough estimate based on visual inspection, plaque volume provides exact measurements of plaque size in cubic millimeters, allowing for more precise monitoring of plaque progression or regression.
- Observer Variability: TPS is subjective and can vary significantly depending on the clinician’s interpretation, whereas quantitative analysis with AI-guided reading reduces this variability by standardizing measurements across different cases, leading to more consistent results.
- Detail of Plaque Characteristics: Semi-quantitative TPS generally assesses the presence and extent of plaque but lacks detailed information on the specific composition and characteristics. In contrast, AI-guided plaque volume analysis can capture intricate details like the plaque’s composition (e.g., calcified or non-calcified), providing deeper insights into potential risk factors for cardiovascular events.
- Resource and Time Requirements: TPS is faster and easier to perform, requiring fewer resources and no advanced software. On the other hand, quantitative plaque volume analysis is more resource-intensive and time-consuming, as it relies on advanced imaging techniques and AI-powered algorithms to deliver accurate and comprehensive data.
Note from Dave: An interesting aside, early into the study there was a concern at one point we might actually have too few patients with baseline plaque to capture adequate progression data. We discussed possible contingencies, even the possibility of splitting the study into two studies. However, within the year there were enormous advancements in AI-guided analyses of CCTA scans which resolved the issue entirely (See Cleerly). These analyses identify plaque volume in every scan.
Preliminary Quantitative Data for MiHeart Match
The following are the Median PV (Plaque Volume) for the Keto-CTA and MiHeart cohorts. (Note: one scan from each could not be processed). For previous Table 1 & 2 values, see Dr. Budoff’s presentation.
Note from Dave: Understandably, these are the data I was most interested, particularly Non-calcified Plaque Volume. There’s quite a bit to say on this, but for now, I’d rather just emphasize we’ll be doing a deeper analysis on this in the coming paper.
Match Analysis Excluding Cholesterol Lowering Medication
Preliminary Quantitative Data for MiHeart Match
Easily the most requested reanalysis since the match was reported by Dr. Budoff was an exclusion of the 26 participants of MiHeart who were on cholesterol lowering medication.
Note from Dave: As with the PV of the original match analysis above, these values are extremely close, particularly our major endpoint of Non-calcified Plaque Volume with each group. Again – and with emphasis – these data are preliminary. Our final analysis will be published soon.
Hello Dave
I’m a sometime-regular participant in the LMHR Facebook page. My non-scientific, laylady hypothesis is that the typical LMHR’s diet is practically devoid of ADDED saturated animal fat. LMHRs typically cook their food. This process removes at least a portion of the embedded animal fat in the meat. And the vast majority of the people whom I have ‘interviewed’ in the FB group do not eat ADDED saturated animal fat.
I think many people fear saturated animal fat, and especially ADDED saturated animal fat.
I’m not necessarily concerned with high LDL and high total cholesterol levels; I’m far more concerned that so many people avoid these heart-healthy animal fats, and that the high-protein diet could lead to insulin resistance.
Georgia A. Ede and Elizabeth Bright both preach the value of saturated animal fat for human health, and especially for female health.
I’m in ALL the carnivore/low-carb/animal-based groups, and I see some issues that make me think of insulin resistance among ‘our’ people: a high A1C, hair loss, and joint pain
Have you done any research on children with low carb diet? I found out my 13 years old boy’s LDL is 600.