We've dealt with this already, Simpson. You are completely scientifically illiterate, and in NO position to comment on this topic:
youtube.com/live/o0c-cc14L1k, your slop positing does NOT affect the facts. Not a jot. Get back in your lane, which is bariatric butcher.
An N=1 is not meaningless. It is how medicine often notices anomalies.
But an N=1 also does not overturn decades of converging mechanistic, genetic, pathological, epidemiologic, and clinical trial evidence linking ApoB-containing particles and LDL exposure to atherosclerosis.
Nick’s result is interesting precisely because biology is complicated. Some people with extremely high LDL develop disease early. Some later. Some appear protected for a period of time. That has always been true. Smoking works the same way — not every smoker gets lung cancer at 40. That does not invalidate causality.
And importantly, children born with even higher LDL levels from familial hypercholesterolemia are not all dropping dead at age 10. What we typically see is accelerated atherosclerosis with premature cardiovascular disease — often major events in the 20s, 30s, or 40s depending on mutation burden, lifetime exposure, and treatment. The biology is cumulative exposure over time, not instantaneous punishment.
We also do not have a complete lifelong exposure history here. We have selected data points and retrospective interpretation. We do not know what his LDL levels were throughout adolescence and early adulthood, what his ApoB burden was over time, what his inflammatory markers were, what his genetics beyond LDL may contribute, or how long he has actually maintained these extreme levels.
That matters, because atherosclerosis is fundamentally an exposure-over-time disease.
So the real question is not:
“Can a person with LDL >500 have little plaque today?”
Of course they can.
The question is:
“What happens to population risk as cumulative ApoB exposure rises over decades?”
That evidence remains remarkably consistent.
And the current LMHR/Keto-CTA work has another limitation people should acknowledge openly: the imaging tools being used were validated primarily in symptomatic or known-CAD populations, not asymptomatic low-plaque individuals where measurement noise becomes a much bigger issue.
So curiosity is warranted. Premature declarations that “LDL doesn’t matter” are not.
Medicine is full of exceptions. Biology always has outliers. But outliers do not erase base rates.