If low LDL or ApoB caused higher mortality, the Mendelian randomization studies would show this, when in fact they show the opposite.
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@Agetron I agree with @CTStan and I would go a step further and say below 60 should everyoneâs target. In your case, a low rosuvastatin, 5mg/day will easily get you there.
Keep in mind, both you and me (I have a zero CAC also), donât have calcification (yet), but we do have arterial damage. There is no doubt about it. If we would do an angio CT, we could see the actual damage accumulated along our life. Minimising AUC going forward should be the goal here.
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Thanks - I appreciate the suggestion and will discuss with my GP. He is very open to my perspective - obviously or I wouldnât be prescribed rapamycin.
But also, that said I am not a fan of statins 
and a few decades older with good numbers. My LDL-C dropped 68 points no changes or medications. Maybe my ApoB is next. Again, appreciate the suggestion. Amazing people on this group!
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Very comprehensive look at coronary calcium screening and its prognostic implications.
- CAC of zero is associated with an excellent outcome for up to 15 years.
- CAC of zero leads to < 1% annual risk of death or non fatal heart attacks.
- CONFIRM study showed < 1% heart attacks with zero score.
- The present European Society of Cardiology study showed a prevalence of 3-8% of obstructive CAD. The test was less reliable in younger age groups. This is apparently due to a higher prevalence of non calcified lesions in the younger groups.
Even so, the annual risk of heart attacks or death remained < 1% with zero scores, even with CAD. This was true even in symptomatic patients. - CAC of zero is an excellent prognostic indicator especially in older age groups and men.
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Mice are better for cancer since they rarely have CAD leading to death.
Itâs very difficult to have a human study ranging over many decades.
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Resveratrol yet again:
@Blagosklonny
(https://twitter.com/Blagosklonny)
Resveratrol protects against atherosclerosis by downregulating the PI3K/AKT/mTOR signaling pathway in atherosclerosâŠ
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" in atherosclerosis model mice" (I wonder how well-validated the mouse model isâŠ)
And n=12 mice on resveratrol.
not a well-powered studyâŠ
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I do believe Dr. Blagosklonny wanders a bit outside of his area of expertise. He does like to post frequently on Twitter. Because of his reputation and education, his opinions are often overvalued due to the âhalo effectâ.
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This is an interesting presentation from a San Francisco company. It was called Underdog Pharmaceuticals (which I loved) but now theyâve renamed to something more conventional⊠Cyclairty Therapeutics.
Their goal is to develop technology to treat, cure, and reverse atherosclerosis
Related:
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Thanks for pointing out this video. The future looks exciting, especially for the younger members of this forum. Younger members who follow the ant-aging field will probably get to live past 120 yrs.
The videos for this summit are very good. One from the Buck Institute suggests that the epigenetic clocks that we have been using are probably worthless and explains why we get such varying results.
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I think atherosclerosis is mainly a consequence of failure to differentiate which can be fixed the same way as osteoporosis and sarcopenia. (much that things like Cholesterol etc come into this as well).
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Could you please give a link to the Buck video. I must admit I am also sceptical about methylation clocks. I think methylation is mainly consequential although it has an effect. It is also prone to quite a range of results from the same sample.
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Non-HDL-c seems important to test with apoB and lp(a). Of which lp(a) is pretty stable and most people only have to test it once or twice, since its hard to lower.
ApoB vs. Non-HDL-c:
An excellent article. Itâs frankly stunning that this topic continues to provide conflicting and contradictory data from studies that are well done. Weâve been looking at cholesterol and its impact on CVD for over 40 years now.
The conclusions drawn here were insightful and very honest , and once again this topic is far from settled. LDL or ApoB? Not yet known.
â APO b is not all informative â. We must consider the ability to both enter and bind to the arterial wall. And it is in this context, as Iâve argued repeatedly, that rapamycin may play a major role in reverse cholesterol transport .
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Sure, but we donât know what those factors are that is influencing apoB to enter the aterial wall and bind to it. So might as well focus on reducing amount of apoB particles and apoB plasma concentration (non-HDL-c) in the meanwhile as the effect can be so massive.
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15 year study in the very prestigious journal Nature once again shows the mortality risk of very low LDL levels.
This is believed due to increased risk of sensory impairment, cancer, and infections.
https://www.nature.com/articles/s41598-021-01738-w
Multiple studies now demonstrate this association. This supports the old study on rodents showing statins causing cancer. This can no longer be tossed aside as merely reverse causation.
The lower the better is looking like a significant risk for all cause mortality. Keep the level in moderation.
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Nothing new under the sun, something else is confounding the result as the genetic mendelian randomization studies show an increase in longevity with lower LDL and the opposite with higher LDL, also in those above age of 90.
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I always find this paper fun to revisit from time to time. Certainly not negative towards statins. I still donât take them, but if my LDL cholesterol were to rise, I would consider them.
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I am not advocating the use of statins, but because of the numerous studies with very large cohorts for decades, I think that if it was a significant risk it would be obvious by now.
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