Thanks for all the engagement, let’s see if I can clarify.
The 50% reduction would be a lifetime reduction for people starting in their 20s and 30s with no obvious risk factors.
The 50% number has been pulled out of thin air, but a number that seems plausible to me. When I say plausible, I mean that given what I have read so far, it wouldn’t surprise me if that was the case.
There is indirect evidence based on the PCSK9 genetic mutation, but like you said, this doesn’t guarantee that you would achieve the same results by lowering LDL-C artificially. But, it does make it more plausible.
Mechanistically, it also seems plausible to me, because plaque accumulation happens over the span of 4 decades.
Your meta analysis doesn’t push back on this number, because it does an analysis over a relatively short treatment period. Its selection criteria are a treatment period of at least one year and a follow-up of six months. As far as I’m aware there doesn’t exist a trial with a 10-year period or longer. What I’m discussing here, when I say the 50% number, is a 60 year treatment period.
I wish I could give a number for lifetime treatment of atherosclerosis in a population with no obvious risk factors, because that is exactly what I’m looking for!
Hey, I think you are right. I myself am doing my Masters in Nutrition and Biomedicine and have been reading up a lot on preventive cardiology (lipids, statins, etc.) over the last few months. Here are some more papers that I think are good and may be helpful for argumentation:
https://pubmed.ncbi.nlm.nih.gov/28444290/ (Probably the most influential paper on the topic of LDL and atherosclerosis—a consensus statement from the European Atherosclerosis Society).
In addition, leaders in the field like Thomas Dayspring or Allan Sniderman (you cited some papers of his anyway) are good places to go for information (e.g., the podcasts with Peter Attia, which you may already know anyway).
Personally, I’m still under 30 and have “optimal” non-HDL-C levels according to guidelines, but I’ll probably take a low-dose statin to get to under 100 mg/dl or LDL-C under 70 mg/dl or ApoB to about 60 mg/dl. At least for me, that is not achievable with lifestyle alone.
In addition, Lp(a) is still an important point. This is genetically determined and cannot (yet) really be influenced, but with a high value the treatment should be all the more aggressive.
Thanks for all the engagement, let’s see if I can clarify.
The 50% reduction would be a lifetime reduction for people starting in their 20s and 30s with no obvious risk factors.
The 50% number has been pulled out of thin air, but a number that seems plausible to me. When I say plausible, I mean that given what I have read so far, it wouldn’t surprise me if that was the case.
There is indirect evidence based on the PCSK9 genetic mutation, but like you said, this doesn’t guarantee that you would achieve the same results by lowering LDL-C artificially. But, it does make it more plausible.
Mechanistically, it also seems plausible to me, because plaque accumulation happens over the span of 4 decades.
Your meta analysis doesn’t push back on this number, because it does an analysis over a relatively short treatment period. Its selection criteria are a treatment period of at least one year and a follow-up of six months. As far as I’m aware there doesn’t exist a trial with a 10-year period or longer. What I’m discussing here, when I say the 50% number, is a 60 year treatment period.
I wish I could give a number for lifetime treatment of atherosclerosis in a population with no obvious risk factors, because that is exactly what I’m looking for!
Hey, I think you are right. I myself am doing my Masters in Nutrition and Biomedicine and have been reading up a lot on preventive cardiology (lipids, statins, etc.) over the last few months. Here are some more papers that I think are good and may be helpful for argumentation:
https://pubmed.ncbi.nlm.nih.gov/28444290/ (Probably the most influential paper on the topic of LDL and atherosclerosis—a consensus statement from the European Atherosclerosis Society).
https://www.sciencedirect.com/science/article/pii/S2666667722000551 (Very good overview including line of argument for earlier and more aggressive treatment)
https://pubmed.ncbi.nlm.nih.gov/15172426/ (Optimal LDL levels)
https://pubmed.ncbi.nlm.nih.gov/29241485/ (Linear relationship between LDL-C and atherosclerosis even in the “normal” range)
In addition, leaders in the field like Thomas Dayspring or Allan Sniderman (you cited some papers of his anyway) are good places to go for information (e.g., the podcasts with Peter Attia, which you may already know anyway).
Personally, I’m still under 30 and have “optimal” non-HDL-C levels according to guidelines, but I’ll probably take a low-dose statin to get to under 100 mg/dl or LDL-C under 70 mg/dl or ApoB to about 60 mg/dl. At least for me, that is not achievable with lifestyle alone.
In addition, Lp(a) is still an important point. This is genetically determined and cannot (yet) really be influenced, but with a high value the treatment should be all the more aggressive.