Lowering LDL isn't equivalent to a seatbelt. A seatbelt is a safety device that performs a function in an accident.
LDL is used as a predictor because it is easy to measure not because LDL itself causes heart disease. Lowering LDL doesn't actually do anything on its own, because it is just a proxy metric for the underlying problem.
It's more cranky to shutdown discussions by misrepresenting someone's position as "cholesterol denialism". What does that even mean in this context? Finding better predictors is denialism. Great now we just need a ministry of truth.
>Lowering LDL doesn't actually do anything on its own
Is this some sort of weird philosophical statement? Because, of course, it's completely nonsensical, and completely at odds with all data on this file.
Lowering LDL reduces CVD incident rates, with no other interventions. People with genetically low LDL also have lower CVD incident rates. This is extraordinarily well proven.
So it sure seems -- you know, 100% of medical science -- that lowering LDL does "something".
The human body is a complex machine, however, and CVD is multifactorial, and for CVD to develop the current thinking is that you need inflammation and high cholesterol over decades. Inflammation can be caused by things like high blood pressure and the like. But everyone has inflammation to some degree as a facet of living, and the easiest component of that to treat (not just measure) is LDL.
And yes, there is an industry of cholesterol denialists, among whom there are just loads and loads of chiropractors. These clowns have built armies of poorly informed disciples that run to HN to tell us that cholesterol doesn't matter and lowering LDL doesn't do anything.
> People with genetically low LDL also have lower CVD incident rates. This is extraordinarily well proven….. you need inflammation and high cholesterol over decades.
We know that low LDL does not prevent CVD. Therefore we know that you do not need high cholesterol over decades.
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.
LDL is used as a predictor because it is easy to measure not because LDL itself causes heart disease. Lowering LDL doesn't actually do anything on its own, because it is just a proxy metric for the underlying problem.
It's more cranky to shutdown discussions by misrepresenting someone's position as "cholesterol denialism". What does that even mean in this context? Finding better predictors is denialism. Great now we just need a ministry of truth.