I have a tough time using mendelian randomization as the final step required to meet a causal requirement for two reasons, Firstly, while it claims to eliminate confounders, that would not be true in an environment whereby a large proportion (say 60% or more) of a population followed a set of dietary guidelines provided to them or more eating a SAD. If a higher ldl showed an issue with this group of people, it may be a secondary response to the poor metabolic health. Hard for me to eliminate the predominant dietary program as a confounder. Secondly, I find the Bradford Hill criteria in general to be insufficient to guarantee a root cause as opposed to actively involved and thereby defined as causal. As a possible example, suppose that people with very high ldl have an injury rate higher than the resolution rate such that soft plaque begins to form. As many note, if ldl is the ambulance, then perhaps, much like an allergy is an immune system over-reaction, the ldl over-reacts to the injury and thereby too many ldl attempt to clean up the issue and end up causing morer plaque buildup than in those with a lower LDL. LDL could then be defined as causal by the criteria, but yet not be a root cause, as it is only a reaction to a root cause. I have a set of over 700 papers on heart disease I am using for my deep dive. Well, or I was in the process, but now that I JUST got a CCTA showing zero soft or hard plaque with zero CAC, it is hard to stay motivated to complete the reading to become fully versed enough to defend my positions with multiple published links (atm).
Discussion of dietary cholesterol and cardiovascular disease
There is definitely some irony in the fact that people who do keto probably have some of the highest levels of LDL with arguably lower incidence of ASCVD. I get what you’re saying in that environmental factors that cause damage to artery walls are more the culprit in this disease. So, while generally the higher your LDL, the more likely it is that there will be plaque build up, if you have no damage to fix, then the LDL won’t have any reason to exacerbate it. So “causal” here is somewhat of a hype word. I shouldn’t take credit for that either, it was from Peter Attia’s podcast that I took it 
While a positive correlation (more A <–> more B) cannot by itself establish proof of causality, a negative correlation (more A <–> less B) is sufficient proof of non-causation. So the fact that there are people with high LDL running around who have no cardiovascular disease is pretty good proof that LDL does not cause cardiovascular disease.
A fact that I find intriguing is that something like 75% of people who show up in the emergency room with their first heart attack have either normal or low LDL. To me, this means that their cardiovascular disease could not have been caused by their LDL. Of course, a statin manufacter looks at that statistic and says, “See? It’s deadlier than we thought! Everyone should be using our product.”
Oh my, the man with maybe the highest level of cognitive dissonance…ever? Listened to a podcast when he had discussed a woman with extremely high LDL yet a zero score on a CAC scan (meaning a low level of atherosclerosis), yet said – literally a minute later – “But we know LDL causes atherosclerosis”. Ah, what?
I stopped listening to him after that.
Being eager to learn what I can from the links provided above, I admit to being a bit stymied by this opening sentence from the second paper cited above (after the first one blew well over my head) …
"There can be no doubt now that there is a continuum of in-
creasing risk for complications of atherosclerosis when plasma
cholesterol levels exceed 160-180 mg/dl. Many types of ex-
perimental and clinical evidence substantiate the "cholesterol
hypothesis."
Perhaps I’ve missed a beat, but I thought the “cholesterol hypothesis” has been sufficiently debunked? 
There is a correlation between high cholesterol, but that is not causation. There are people running around with “normal” cholesterol levels, and heart disease. I believe the correlation is because abnormal LDL is being confounded with native LDL.I believe oxidized LDL or oxLDL is the primary cause of most heart disease seen currently. I don’t know where that quote came from, but risk is not causation. I do not worry about my cholesterol numbers at all - other than trying to keep my oxLDL levels down, because I believe science has sufficiently implicated oxLDL in the disease process. It has been found in the foam cells which start the plaque process. It is why the macrophage shows up. This is now clear from the science.
My own belief, though I doubt I could justify it, is that even oxidised LDL is associated with cardiovascular disease, but not causal.
I suspect that Ravnskov and Diamond are on to something when they identify the causal factor as hyper-coagulability of the blood, because the same factors that increase the coagulability of the blood also increase the oxidation and glycation rates of everything else, as well.
But so long as we consider glucose our friend and fat our enemy, our interpretation of the data will be distorted to fit that belief.
Fully agree, based on my reading of seemingly reliable studies. (The quote is the opening of one of the papers you cited above.)
I’d agree with your idea. I think the same thing can be said about sub-types of LDL or HDL, as these probably just indicate the person’s diet, and diet likely affects coagulability of the blood. (Though I think I have a genetics issue for HDL for me; my HDL has gone up, but the sub-types of HDL I need to get a good “score” on LPIR have not.)