ng0rge
#298
Hold on, let me get my bot (not named vlasko) to start firing off studies about why ApoB is a better measure than LDL…cuz we all know it is.
ng0rge
#299
Here’s a carefully hand-picked article that is short and to point (but nothing new).
“If the amount of cholesterol per particle was always the same, measurements of your cholesterol values (LDL-C and non-HDL-C) and your particle numbers (LDL-P and ApoB) would give very similar results. However, because the amount of cholesterol carried inside lipoprotein particles is highly variable, cholesterol tests and particle number tests frequently show conflicting values with regard to your cardiovascular risk. In statin intervention trials, apoB levels on therapy are a significantly stronger predictor of cardiovascular event reduction versus LDL-C or non HDL-C. Your LDL-P and ApoB particle score is your best reference point to track your cardiovascular risk.”
https://precisionhealthreports.com/ldl-p
1 Like
AnUser
#300
I said almost the same thing. ApoB is superior, of course.
ng0rge
#301
This study is also interesting. - “Discordance between LDL-C and Apolipoprotein B Levels” - They divided the study participants into 4 groups with LDL-C and ApoB scores.
“group 1 (low LDL-C, low ApoB), group 2 (low LDL-C, high ApoB), group 3 (high LDL-C, low ApoB) and group 4 (high LDL-C, high ApoB).”
Particularly see group 3, even with high LDL-C, it’s the low ApoB that accounts for a good outcome.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8781725/
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Sorry. Missed it. Here it is.
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Neo
#304
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adssx
#305
Does this suggest that CVD is a disease of ageing and that maybe it’s not about ApoB levels per se but early intervention to slow down the ageing and restore some functions (reverse cholesterol transport?)?
4 Likes
I don’t think there is any doubt that CVD is a disease of aging, but it also appears to be exacerbated by high levels of ApoB.
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I believe that CVD has two important variables that affect it - ApoB and inflammation. Both increase as you age. Both are also alleviated by Bempedoic Acid and Ezetemibe. Rapamycin also reduces inflammation.
Of course this is just a simplified version as there are many other factors involved but I believe these two are the biggest for CVD.
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adssx
#308
Inflammation as measured by which marker(s)? And how does bempedoic acid/ezetimibe compare to statins on this?
2 Likes
Inflammation as measured by hsCRP. The literature says BA reduces hsCRP by 20%. For my father, it was reduced by 66%.
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adssx
#310
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AnUser
#311
LDL-c causes heart disease via apoB, independent of any pleiotropic effect of a medication like statins.
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Yes, I understand it’s particle count and time (age). No doubt other variables are in play but high apoB times many years is enough to kill a person most of the time.
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Neo
#313
Could be as simple as massive lowering of Apo B dominates any (smaller) hs-CRP increase?
How big is the CRP increase with those? (My hs-CRP on now full dose repatha is still below the lowest threshold of the test so I don’t know if mine has changed).
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AnUser
#314
I think that is the case. Statins increase Lp(a), as well, but still have a worthwhile effect (probably primarily) due to the decrease in apoB, and hs-CRP and other pleiotropic effects contribute some.
4 Likes
L_H
#315
This is interesting. Psk9 inhibiting genes have lots of pleiotropic benefits
“Investigations in animals and humans suggest that the impact of PCSK9 inhibition is not limited to reduction in LDL-C but also affects other aspects of lipoprotein metabolism, inflammation, thrombosis, and immune function.”
https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.116.023687
3 Likes
AnUser
#316
If that is the case then few young people should have atherosclerosis, same source as above:
“We know that atherosclerosis begins early in life. In fact, a study from the 1990s looked at 111 casualties of the Korean War who died from non-cardiac trauma. 78.3% of these relatively healthy individuals with a mean age of 26 years showed coronary atherosclerosis. Over one-fifth had greater than 50% narrowing and just as many had left main or significant two and three-vessel involvement suggesting that ASCVD begins much earlier in life than usually presumed [58].”
I don’t think atherosclerosis has much to do with aging, it is proven it has everything to do with time and exposure to sub-optimal levels of apoB.
How do you know whether something is an age or time based disease?
Suboptimal levels of apoB have large effects with time. That’s all you need to know, practically.
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How do you explain that some people with familial hypercholesterolemia die or have advanced disease in their thirties and some with same level of lipids have no sign of ASCVD into the old age?
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