It's like saying a flying bullet can't do anything on its own. It is a meaningless statement.
>As I pointed out in another post over 75% of people who have heart attacks have normal LDL.
The actual study authors were advocating for lower LDL guidelines, particularly among the elderly.
A heart attack is the destination, not the journey. What someone's LDL was at admission for a heart attack says literally nothing about their state for the decades before. In actual studies tracking cholesterol, even over a five year period lowering LDL has a potent beneficial effect.
>You’re saying a lot of nonsensical stuff in your comment like high blood pressure causes inflammation , which tells me you are not serious in this discussion
Hypertension can cause endothelial inflammation, leading to blood vessel damage and promoting the release of inflammatory mediators. This is extremely well documented, and it's why getting hypertension under control medically is considered extremely important in the CVD battle. Inflammation and hypertension often are found hand in hand, and there is uncertainty over the cause and the effect, but strangely controlling hypertension alone dramatically reduces inflammation. Weird, right?
>I have zero inflammation
Sorry, but LOL. Not only is that a singular and very narrow test, inflammation is literally just a facet of living. As is oxidization. There isn't a single human alive with "zero inflammation", nor is there anyone that has magically non-odidizing LDL.
If you don’t understand the difference between acute and chronic inflammation, there is no longer any reason to continue this conversation with you. Yes, I apologize because I didn’t specify the difference, but I thought you would be intelligent enough to know the distinction.
Localized foam cell activation and cytokine signaling does not necessarily raise hsCRP yet allows for continue plaque deposition. This is a very well understood mechanism.
No one knowledgeable here is saying that inflammation isn't worth paying attention to, but people acting like because inflammation is also important that LDL does nothing just aren't living in reality.
Your comment about blood pressure actually reveals more about your knowledge here than the person you're replying to.
FDG-PET is a signal we can use to detect tissue inflammation, and we know that higher blood pressure is highly correlated with increased FDG-PET in arterial walls:
Blood pressure results in shear stress to your arteries. This results in several things that amplify Angiotensin II and NF-kB activity, including expoosing adhesion molecules which then results in foam cell activation and cytokine signaling, etc.
It is quite well established that high blood pressure will contribute to increased inflammation.
