Well, after decades of ridiculous monofocus on ‘cholesterol’ (the secondary interacting contributor to CAD (yes, I’m including LDLp), largely irrelevant unless you are afflicted by Insulin Resistance anyway), let’s hand it over to the highest science for a moment. Yes, let’s hand it over to the mathematicians. Remember that the hypertension and cholesterol-related contributors are largely driven by the same crap that drives IR in any case. Also, gut health and infectious agents that are purported to speed atherosclerosis progression are also going to be driven by what puts you in a hyperinsulinemic state. The insulin elephant stomping around the room for the past 50 years, while everyone was flogging (still is flogging) the cholesterol horse to death. Reaven was, and is, correct.
The Big Picture:
And a timely reminder of Reaven’s 2001 sample of 208 healthy middle-aged people properly measured for Insulin Resistance using euglycemic clamp, and split into tertiles of low, medium and high IR; following them for 6 years spoke volumes, small sampling theory covers the validity in spite of moderate numbers used. IR – the primary cause of CAD & most other modern disease – read it and weep:
I propose that this is why some familial hypercholesterolemics die young, others not. Why some T1D’s become very ill, but Dr. Bernstein and others are thriving in their eighties. Why most T2D’s have massive risk, but others reverse all their risk factors with #LCHF, and time will show that they prevail. Why some high Lp(a) peeps are screwed, but others thrive to old age. Same for LDL and LDLp etc. Same most likely for ApoE4 dudes. Why Kitavans with their uber-low Insulin levels has vanishingly low rates of CAD. Etc. Etc. Same for a damn lot of outcome scenarios. Sit back and enjoy the high-level summary below:
Without Insulin Resistance and the associated hypertension / endothelial distress / etc. etc. etc. , even the more adequate measures of ‘cholesterol’ that associate with CHD become largely irrelevant: