If LDL is low but triglycerides are high, with untreated diabetes, that probably means there were discordance between LDL and apoB and apoB was either normal or elevated. Having a normal or high apoB causes disease over time many decades, and diabetes is not good for anything and increases risk.
Just measure apoB…
Just measure apoB…
ApoB does not look like a great replacement for LDL-TG, especially for statin users.
Anyone have these Hart tests by Provencio?
Claims are that 86% accurate at predicting one years heart/ stroke risk
Any independent 3rd party validation of their claims? False positives?
"The Future”: the only marketed prognostic blood test for 1-year risk of heart attack (MI), stroke or cardiac death (MACE or major adverse cardiovascular events). Yielding an accuracy of 86%, HART CVE™ assesses four clinically significant blood proteins in a machine learning (AI) algorithm to calculate a patient- specific risk score. Proteins include:
- NT-proBNP- associated with myocardial (heart) stress
- Kidney Injury Molecule-1 (KIM-1)- associated with cardiorenal dysfunction and injury
- Osteopontin (OPN)- associated with calcification and plaque formation
- Tissue Inhibitor of Metalloproteinases-1 (TIMP-1)- associated with plaque rupture potential and left ventricular enlargement and dysfunction
The Here and Now”: diagnostic blood test for obstructive coronary artery disease. Yielding an accuracy of 86%, HART CADhs™ assesses three clinically significant blood proteins and three clinical variables (age, sex, history of coronary intervention) in a machine learning (AI) algorithm to calculate a patient- specific risk score of obstructive coronary artery disease. Proteins include:
- hsTroponin- associated with myocardial ischemia and injury
- Kidney Injury Molecule-1 (KIM-1)- associated with cardiorenal dysfunction and injury
- Adiponectin- associated with glucose and fatty acid metabolism
Thomas Dayspring have said it’s a surrogate for apoB. If that paper is enough evidence for you, you can always measure both.
This preprint ( Obicetrapib (CETP inhibitor for dyslipidemia) - #130 by adssx ) quantifies the effect of cumulative LDL exposure on cardiovascular risk: HR 0.69 per 10–mmol/L×years; 95% confidence interval, 0.52–0.90; P=0.007
10 mmol/L = 387 mg/dL. So, if you reduce your LDL by 38.7 mg/dL over 10 years, you reduce your cardiovascular risk by 0.69?
Thomas Dayspring have said it’s a surrogate for apoB.
Thomas Dayspring might have said that, but the paper definitely does not. “Adjusting the model for age, sex, LDL-C and ApoB levels demonstrated that the association of LDL-TG with atherosclerosis was independent of these well-known factors [, including ApoB].”
Just look at the chart for the population in the study for ApoB and LDL-TG. You could be patting yourself on the back for having lowered your ApoB < 50 with statins, but your LDL-TG could still be elevated, increasing your CAD risk.
you can always measure both.
I would love to, know how I can get a measure of LDL-TG? I looked at sites like RequestATest.com and couldn’t find one.
Isn’t LDL-TG just a composite marker of LDL-C and triglycerides (which we know are both independently related to CVD)?
If this is the case, since apoB is better than LDL-C wouldn’t apoB and triglycerides together be more predictive for disease than LDL-TG alone?
Looks like that study method is B.S. with a B.S graph.
50 apoB doesn’t have the same risk as 120 apoB. Just another fake U-shape curve with residual confounding.
It would be nice if there was a way to get LDL-TG from TG and LDL-C. I couldn’t find any resource online to do that. FWIW, I asked ChatGPT and got the following.
It is not possible to calculate LDL-TG (low-density lipoprotein triglycerides) directly from a standard lipid panel because such panels typically report:
The triglycerides reported in the standard lipid panel reflect all triglyceride-rich lipoproteins, not specifically those in LDL particles. LDL particles typically contain very little triglyceride, and LDL-TG levels are not routinely measured in standard clinical settings.
To measure or estimate LDL-TG, specialized techniques like ultracentrifugation or nuclear magnetic resonance (NMR) spectroscopy are required. These methods separate LDL from other lipoproteins and allow for direct triglyceride content analysis.
If you’re interested in exploring this, it’s best to consult with a healthcare provider or a lipid specialist to discuss the need for advanced lipid testing.
Formulas are here: Cardiovascular Health - #1451 by adssx
But that’s only the estimated LDL-TG (eLDL-TG). If you want to find your real LDL-TG you need to test it but as you said it’s not commercially available in most labs.
The bottom line is that small LDL particles tend to stick to arterial walls, causing arteriosclerosis.
Large particles do not tend to stick; is this not true? Am I missing the point?
If this is the case, then the best measurement that is commonly available for a reasonable price is:
Here is a real example of my lipid tests taken at approximately the same time.
The conventional lipid tests all fall within acceptable margins.
However, the Lipoprotein Fractionation NMR test shows that not all is well.
LIPOPROTEIN FRACTIONATION NMR:
They tend to stick less than small particles but contain more cholesterol so overall the net effect is the same for both types.
Imagine a cal 50 BMG round hitting you once or 9mm bullets hitting you 10 times. In both cases you’d end up dead.
It’s not the impact that matters most of the time, it’s the amount of bullets, so the 10 9mm bullets would be more harmful to the arterial wall in this context… that’s what apoB measures.
Not sure about LDL particle sizes. LDL-TG is a component of LDL, so maybe LDL size doesn’t matter as much?
Using your lipid values to estimate LDL-TG, I get 31 mg/dL. Per the paper, ideally you would want this below 20. In your case, the main target would be lowering triglycerides. But who knows, the estimate only has a R2 of 60%, so there’s a lot of room for error.
Statin update. It seems I am even intolerant to 5 mg of Atorvastatin. I switched to a Monday-Wednesday-Friday night dosing schedule and the muscle spasms stopped, but I still experience muscle weakness in my calves and thighs on Tuesday-Thursday-Saturday. We’ll see how much this low dose every other day strategy lowers my LDL and ApoB. I may have to skip statins altogether. Bempedoic Acid and Ezetemibe work just fine with no side effects.
My wife doesn’t do very well with statins either. Her doc prescribed 40mg, she kept reducing because of side effects (weakness and forgetfulness), now she gets 5 mg and quarters them, 1.25mg per day (looks like a spec of dust). Despite the miniscule dose, it still keeps her ldl in check.
How long was the LDL at 38? Did she have a high level of LDL before getting it down to 38?
It was always pretty low. The highest I ever heard of for her was an LDL of 68 without any treatment.
Can you describe the muscle spasms in more detail?
