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.
this is often called the plea atrophic effective status or the anti-inflammatory affective Stratton's you may have heard this word it's something we throw about a medicine CLIA trophy the idea that lowering LDL may not be what's really benefiting in terms of statin medications it's quite a controversial topic
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the reason that the statin has an effect on the the secondary heart attack outcomes it's not even because of its effect its intended effect the drug was designed to interfere with the specific means on you've named notice H and G coenzyme a doctor doctor is one thank you pause which actually is if you look at the kink pathway of the metabolic reactions is actually fully two pages above molecular cholesterol and yeah it's not completely and that's it's amazing if people if people look at the cholesterol synthesis pathway and they look at how high up in that pathway HMG co-reductase is and they see all of the molecules that are inhibited in their production when you give a statin they will think wow like don't those other molecules do something important in the human body and they do go into ten does something important among others like it's a big big pathway yep because genes encode for them why are those genes there because those genes have survived in a selection they're there for a purpose Charlie Brown anyway so statins do reduce the serum level of cholesterol absolutely they work they work very well they do exactly what they're supposed to do they on the turn however that's not the reason why the secondary heart attack events are reduced in their population okay so it's actually a confounder all those molecules are get knocked out includes some of the inflammatory pathways no any of us that know anything about it that atherosclerosis heart disease cardiovascular problems of that kind at their root cause as systemic chronic inflammation yeah so what we're saying is it's actually the anti-inflammatory effect of the statin but has the effect it's nothing to do with the effect on the cholesterol which is actually working again anti-inflammatory effect right
that statins really probably do not lower your your cardiovascular risk in secondary prevention trials by lowering LDL and they do it by improving inflammation
if you listen to the podcast to do with malcolm kendrick we talked about this paper which shows that probably the pleiotropic effect of statins has to do with nitric oxide so maybe it's not even ldl reduction with statins that are causing their benefits
what if the actual effect of statins the actual protective benefit of statins in secondary prevention and people who have had a heart attack comes from improving nitric oxide synthesis at the level of the endothelium
it could turn out that the lowering of LDL for something like statins isn't actually the agent of value it could in fact be that that's a side effect of what is otherwise providing an agent of value for people with secondary prevention such as uh modulating the inflammatory outcome more or you know greater nitric oxide expression or something along those lines
statins do have some pleotropic effects in the sense that they have anti they have antioxidant effects they have some anti-inflammatory effects and it's somewhat arguable that the benefits of them are through those Pathways and not through LDL lowering
the sort of hypothesis is well all of the statin benefit doesn't come through the LDL reduction through the mechanism you describe the unintended consequences the wrong way of saying it but the non-obvious consequence but it could be some of the anti-inflammatory benefits that come from it or you know the endothelial protective benefits