The dismissal of anecdotal data is why science has been stalled and people are still sick.
The fact that you don’t care if one person who has high, LDL does not get heart disease is emblematic of the problem in healthcare. If one person who has high, LDL does not get heart disease then high LDL alone does not cause heart disease. There is amounts of evidence that LDL on its own, when it is not oxidized by inflammation, does not cause heart disease is something you’re consistently overlooking.
Again, and I don’t know why I have to repeat this, but I know that Laura LDL decreases cardiovascular disease risk, but that is only because if you have lower amounts of oxidized LDL, then you won’t get heart disease. But what do we want to lower, the LDL, which is needed by the body or the oxidative stress and inflammation which damages the LDL we need for our body?
High LDL or Lp(a) on its own causes enough localized inflammation to continue plaque deposition. We can’t drive down every cause on inflammation to 0 to the point that there is zero plaque deposition at all in the presence of high LDL, there are just too many causes. Even temporary increases in inflammation from natural processes can deposit plaque is you have high amounts of atherogenic particles. And once they deposit, they begin to cause inflammation independently. Not all inflammation can be measured by hsCRP.
Inflammation is an important causal factor for sure, and persistent high levels of inflammation will drive even more deposition of plaque.
Your body does not need serum LDL in significant quantities. I’ve commented in this post multiple times with studies that show that even driving LDL down below 20 has no impact to the systems that use LDL that people are concerned about. All of the related organs can do de novo synthesis, make use of HDL instead, etc. People that do not produce LDL at all that ends up in the bloodstream still produce all of their necessary hormones at normal rates, the brain still produces it locally de novo, etc.
No one thinks LDL and Lp(a) are the sole factors in heart disease. We know of plenty that are unrelated - blood pressure, LVH, etc. etc. etc.
But lowering LDL is one of the most powerful and broad spectrum tools we have at our disposal.
The fact that you don’t care if one person who has high, LDL does not get heart disease is emblematic of the problem in healthcare. If one person who has high, LDL does not get heart disease then high LDL alone does not cause heart disease. There is amounts of evidence that LDL on its own, when it is not oxidized by inflammation, does not cause heart disease is something you’re consistently overlooking.
Again, and I don’t know why I have to repeat this, but I know that Laura LDL decreases cardiovascular disease risk, but that is only because if you have lower amounts of oxidized LDL, then you won’t get heart disease. But what do we want to lower, the LDL, which is needed by the body or the oxidative stress and inflammation which damages the LDL we need for our body?