The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
elevated blood pressure hypertension is a mechanical disruption to the endothelium smoking is a chemical disruption to the endothelium and of course apob is the concentration of the lipoprotein that itself goes through that disrupted endothelium and then causes the pathologic sequence of events that we're very familiar with
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Native comments, Twitter mentions, and Reddit threads about this claim — surfaced together so the conversation isn't fragmented across platforms.
Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
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the second thing you have to do is you have to protect your endothelium so anything that aggravates and weakens and makes the endothelium more vulnerable to penetration by apob is problematic and the most common factors that we think are doing that are smoking blood pressure and very likely the metabolic conditions that cluster with insulin resistance hyperinsulinemia um and uh type 2 diabetes
and and and probably worth noting Tom that's almost assuredly where things like smoking and high blood pressure make your odds worse those are things that are damaging the endothelium making that barrier more permeable which is simply a probabilistic game this is all probabilistic what increases the odds of an apob getting in more particles that's higher apob more por endothelium that's what happens with smoking that's what happens with um high blood pressure that's in my view probably what happens with things like high homocysteine High insulin or renal insufficiency high uric acid all of those things