3) dozens of randomized trials show near-linear relationship btw LDL-cholest lowering and risk of heart disease
4) people with genetically low LDL-cholest have low risk
1 + 2 + 3 + 4 = VERY strong case
Eur Soc Cardiol: "there is no longer an ‘LDL-Cholesterol hypothesis’, but established facts that increased LDL-Cholest is causally related to atherosclerotic CVD & that lowering LDL particles and other ApoB lipoprots as much as possible reduces CV events"
nonHDL cholesterol is another predictor metric commonly used
nonHDL= Total cholest - HDL-cholest
good predictor. often better than LDL-C. but causality ultimately tracks best with ApoB
ok what about HDL? is it 'good cholesterol'?
population studies suggested positive association (HDL-cholest level inversely correlated with heart disease)
causal tests (higher HDL-cholest via drugs or genetics) did not lower risk
HDL-cholest may be just a marker
analysis of 39 trials: “observational studies might suggest a simplistic hypothesis for HDL-cholesterol: that increasing its levels reduces CV events. But substantial trials do not support this concept”
Re: heart disease in particular, we can find heterogeneity in the literature. Some studies point to a signal of risk for eggs, others find no stat sig effect.
One of the main differences between science and Social Media content is how they deal with heterogeneity.
Social Media feeds you polarization. One FB forum argues eggs are poison, and shows you only the studies reporting risk.
Another argues eggs are a perfect, risk-free superfood, and shows you only favorable studies.
over 2 months, he lost 27lbs. his BMI came down to the normal range
his LDL-C dropped 20%. his triglycerides, 39%
his anecdote illustrates a couple points:
▶️we can lose weight on almost any type of food, as long as we cut calories enough
▶️ some foods make it easier to cut calories. calorically concentrated junk food makes it easier to overconsume calories, so for most people they're not ideal. most people won't achieve the precise control on a day to day basis that the Prof exercised in his experiment
Does high ApoB still raise risk if I´m “metabolically healthy”?
The evidence indicates it DOES.
(thread)
The idea that cholesterol level is completely irrelevant has largely subsided.
As the public is exposed to more scientific evidence, it has become increasingly obvious that blanket denial is not realistic.
So a more nuanced idea emerged.
“it´s about context”
According to this idea, high cholesterol/apoB increases risk in “sick” people (e.g. insulin-resistant/obese/diabetic) but is harmless for the insulin-sensitive & lean
00:32 brain cholesterol is separate from plasma; most cholesterol in the body is inside cells, not in bloodstream; most cholesterol in blood is in RBCs, not lipoproteins ▶️ so reducing serum cholesterol has little to no effect on cellular cholesterol requirements
00:36 it's not cholesterol in the arterial wall that poses a problem, it's trafficked cholesterol inside lipoproteins (digested by macrophages)