You mean the positive impact of consuming statins. Consuming statins coincides with lower LDL so I can imagine people conflating the two variables. I'm sure taking statins also has other effects on the body.
No, I mean the positive impact of lowering LDL. Statins of course show positive impact, and yes, including from also lowering inflammation. But so do other drugs that lower LDL through other mechanisms, including ezetimibe, bempedoic acid, and pcsk9 inhibitors. MR studies on genetics also show that lower LDL even without other factors that reduce inflammation significantly reduces the risk of of negative ASCVD outcomes.
Even from the inflammation standpoint, we know that lowering LDL has a causal effect on lowering inflammation in your arteries - plaque being deposited results in foam cell activation and cytokine signaling which directly increase localized inflammation which can then result in additional plaque deposition.
This is also just extremely well understood mechanistically - to have plaque deposited in your arteries, you have to have something that deposits it. This comes primarily from LDL in most individuals - though Lp(a) is a largely genetically driven carrier of atherogenic particles as well, which is why ApoB is a better measure - and with less LDL there is simply less to be deposited.
The idea that LDL is not a directly causal factor for ASCVD is one goes against mountains of evidence and the consensus of the absolutely overwhelming majority of experts in the field. That is not the same as them saying it is the only causal factor - but people trying to argue that LDL isn't causal have a huge burden of proof on them. This is some of the most studied science in health.
Even from the inflammation standpoint, we know that lowering LDL has a causal effect on lowering inflammation in your arteries - plaque being deposited results in foam cell activation and cytokine signaling which directly increase localized inflammation which can then result in additional plaque deposition.
This is also just extremely well understood mechanistically - to have plaque deposited in your arteries, you have to have something that deposits it. This comes primarily from LDL in most individuals - though Lp(a) is a largely genetically driven carrier of atherogenic particles as well, which is why ApoB is a better measure - and with less LDL there is simply less to be deposited.
The idea that LDL is not a directly causal factor for ASCVD is one goes against mountains of evidence and the consensus of the absolutely overwhelming majority of experts in the field. That is not the same as them saying it is the only causal factor - but people trying to argue that LDL isn't causal have a huge burden of proof on them. This is some of the most studied science in health.