It always did... even the way cholesterol recommendations have been aren't really good in and of themselves. The better marker is Triglyceride to HDL ratio, in terms of correlation to morbidity. Not total, not LDL by itself without quality tests.
Trig/HDL and LDL/HDL ratios are outdated science that have been superseded by our better understanding of the causative factors and our ability to drive LDL way lower than we could in the past.
MR studies have shown very little evidence higher HDL does much, if anything, to prevent CVD or serious adverse events.
CETP inhibitors keep getting abandoned because they're not seeing improvement in cardiovascular outcomes, despite significant increases in HDL. One of the few that did show improvements in outcomes, anacetrapib, appears to have done it through a more significant reduction in LDL than the others, but even then, it was not promising enough for Merck to continue development, and it has since been abandoned.
The current CETP inhibitors still in development such as obicetrapib are focused primarily on their ability to lower LDL rather than raise HDL.
MVMR studies are also quite clear that absolute atherogenic particle count - primarily LDL-C/Lp(a) - are far more important than HDL #s. ApoB, which calculates the total of your atherogenic particles is probably the best marker we have.
For a while we thought looking at sdLDL in particular might be a more specific signal to look at, since these are more atherogenic than larger LDL particles, but we've found they correlate so strongly in the vast majority of cases that it's really only something that matters as an exception rather than the rule
I get ApoB is a better marker... but it's been hard enough in my limited experience to even get the numbers for Tg and HDL from lab results from the doctors I've seen.... they tend to just go "number high, give drugs"
Risk being higher when Tg is more than 2x HDL in adult men. Even then, I'm not sure that medication as intervention is always the right answer vs lifestyle changes, which are of course harder.
My point is that the ratios are no longer considered relevant because we now understand better that HDL itself is not a particularly useful indication of anything - high HDL doesn't help you if your atherogenic particles are also high. All the clinical guidelines these days from places like the NLA, AHA, ACC focus basically entirely on lowering LDL (and will likely focus on lowering Lp(a) for relevant populations once drugs currently in the pipeline are available)
TG/HDL ratio is useful in one place, though - it's a reasonably good screen for insulin resistance if your labwork doesn't include more direct measures.
As for lifestyle intervention vs. medication - lifestyle changes are maybe enough if you're young. Like, in your early to mid 20s young. Plaque is a lifetime accumulation thing, and it's not like it waits until you're old to start accumulating, and while soft plaque can regress, it takes very low levels of LDL - sub 50, and similar with Lp(a). Not sure what the target is for cumulative ApoB. By the time you're diagnosed with ASCVD the treatment target for your atherogenic particles is lower than you can achieve with lifestyle changes alone, and requires medication. And there's a lot of data, such as was examined for the latest NLA recommendations that treatment targets should probably be even lower and people on statins or other therapy for them even sooner. We've relied on CAC as an indicator for a long time because they're relatively cheap and easy in comparison to things that actually pick up soft plaque, but soft plaque can and does still block your artery and can rupture, and even most people with dangerous levels of soft plaque will score a 0 on a CAC up until their 40s or 50s.
We also just know that lifestyle changes just don't work. People don't do them. So even if you're otherwise a candidate because of age, etc., the doctor should still almost certainly be recommending medication - and then if the patient really believes they can make the change, they can decline.
