Super interesting, and I don’t want to turn @alex_uk’s log into a cholesterol debate symposium, but I do like your explanations.
I think the Omega 6:3 suboptimal ratios and corresponding metabolic disease in the Western diet is well-established - totally onboard with you there.
Conventionally-raised chicken as a major culprit is not something I’ve really hear or considered, but there’s no reason for me to really doubt or take that one on. I think your reasoning is sound. I will say, for sake of argument (I suppose I can’t help myself), the standard bodybuilder diet is going to be chicken breast… I think it would be relatively easy (compared to other foods) to “beat” that fat ratio with higher-quality fats. This becomes largely semantics, though, because I’m going to say add a bunch of avocado or fish oil or fatty fish, and you’ll easily counter with a common sense “why not just eat the grass-fed beef to begin with?”… which was the whole point, so touche.
What is interesting, and I probably differ in theory but not practical advice, is the thoughts around LDL accumulation. You’re 100% correct that LDL is there to go heal injury. The theory of athersclerotic cascade to which I’m most likely to prescribe differs slightly here, though. Yes, we likely produce more LDL to heal inflammation, but we’ve got LDL floating around in the bloodstream, anyway. It also becomes a question of “so what” (doesn’t everything?). Like I’m totally fine to have a serum level of 96 running around in there, but when I eat a dessert (typically a bigger deal even than our crappy fats!) and hit 103 I’m going to die unless we get that statin intervention in me right now? Obviously not. So the LDL itself is not the problem, it’s the plaque buildup (that calcifies, restricts arterial blood flow, and ultimately leads to thrombus formation or ischemia). So now we can talk about “well, how does that form? That’s what I care about.” Right we are!
So what am I actually trying to say? It’s LDL’s impact that matters. So our little LDLs are floating around in our bloodstream looking for problems to solve (as you pointed out, they are there to help our inflamed little bodies). Think of them as little ambulances looking for car crashes to go help. Those car crashes are arterial insults - microtears, deformations, etc. We don’t want a microtrauma to eventually become a dissection, obviously, because we’ll bleed to death. Our little LDL ambulances go plug that hole, to prevent that problem. In doing so, though, they begin the atherosclerotic cascade - we’ve got a spot for other cholesterols to attach, we begin to form plaque, harden, calcify, restrict, etc.
Bringing all that home, we now get to “what do I do?” That’s where my whole diabtribe becomes simply academic, because we have the same practical recommendations: don’t eat crap. I would argue that garbage sugars are every bit as concerning as Omega 6:3 ratios, because they do seem to cause arterial insult, but your diet recommendations takes care of that anyway.
