Well then let's just hope it's the result of "I'm taking care of my cholesterol, I should start exercising too.".
One of the problems with this whole field is that the medical community tends to want to treat or prevent MACE rather than prevent ASCVD where one is simply the symptom of the progression of the other.
One of the reasons that prescribing guidelines for statins are so ridiculous is because the clinical trials were in populations that were otherwise very certain to die. This increased the likelihood of the trials being successful and also it would have been unethical to use anything but the maximal dose in that population. So, here we are where lots of younger, otherwise healthy people are accumulating plaque burden and nobody knows how to prevent it even though the interventions to do so are right in front of us.
On the first run of the ski season last year a friend had his Achilles rupture and he has been on statins for years and was in the gym regularly till then. which supports what i have read over the yeas.
The plural of anecdote is not "data". It would be foolish of me to assert that there is no issue, but this is a topic that has been studied ad nauseum that has yielded no definitive answers.
It may not even be more life as the Dr.s appear to have no data showing statins on the average lead to any longer of a life span then if they are not taken.
This is patently false. For one, most medical doctors have no fucking clue about this stuff, but the folks doing the actual research have shown substantial benefit. It appears that you are parroting a statement that's commonplace in the keto/carnivore community which is the product of an inability to interpret statistics.
Are you saying that the new medication is a large enough molecule that it can not pass the blood brain barrier?
Hydrophilic statins, rosuvastatin and pravastatin are not new. They have very little ability to cross the blood brain barrier. Much of the literature on the effects of statins on the brain fails to make that distinction. It is typically based on atorvastatin, which is lipophilic and happily crosses the blood brain barrier.
PCSK9 inhibitors block molecules that would occupy LDL receptors, so LDL can activate them instead, resulting in a downregulation of LDL production via the natural feedback systems intended to keep LDL in check. I suspect this natural cholesterol feedback loop does not interfere with the brain's own capacity to make critical fatty acids.
Not exactly. The PCSK9 protein degrades the LDL receptors in the liver. By inhibiting PSCK9, there are more LDL receptors which increases the clearance of LDL. It is an excellent choice for patients that are statin-intolerant.
Since we're on mechanisms of action:
Bempedoic acid inhibits ATP-citrate lyase, an enzyme used for cholesterol synthesis in the liver. It has two mechanisms of action, inhibiting LDL production in the liver and upregulating LDL receptors. As such, pairs well with a PCSK9i and is another excellent choice for statin intolerant. It is not activated in muscle tissue which presumably reduces the likelihood of any muscle related side effects.
Ezetimibe blocks cholesterol absorption in the small intestine which limits the supply of cholesterol to the liver which reduces the production of LDL. Most folks (in the medical community) presume that the cholesterol lowering effect exists primarily in the small intestine, but in actuality by limiting the supply of cholesterol to the liver, the liver increases the expression of LDL receptors further increasing uptake of LDL from the bloodstream. If this sounds complementary to the two other molecules described, it is. If it also sounds like a great option for statin-intolerant, then you'd be correct.
I'm going to skip providing more detail on statins. That's a contentious topic and there's lots of bullshit to debunk there. They do have issues, but are also incredibly efficacious.