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Instead of basic linear / bell/U curve type ways of describing impact of biomarkers, are new ways of describing complex biomarker relations emerging into the vernacular? e.g. optimums within clusters/sets of biomarkers
Can someone tl;dr? Not that the paper is too long, but I think I'd need to go back to university and major in biology or statistics to understand what they discovered and more importantly what it might mean.
This is not a new finding. It's common enough to have a name: the cholesterol paradox ( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6374572/ ). Also replicated in a more recent n=100k Denmark study: https://www.bmj.com/content/371/bmj.m4266 These are all observational studies, meaning cause and effect is not established. It's relevant that people with some cancers will have very low cholesterol (the cancer apparentl…
This is not a new finding. It's common enough to have a name: the cholesterol paradox ( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6374572/ ). Also replicated in a more recent n=100k Denmark study: https://www.bmj.com/content/371/bmj.m4266 These are all observational studies, meaning cause and effect is not established. It's relevant that people with some cancers will have very low cholesterol (the cancer apparentl…
That's very informative, thank you.
Am I the only one that seems to think there is some correlation is not causation here with the numbers?
No, scientists have studied this phenomenon for decades. This is a study specifically interrogating the direction of causality for low cholesterol and mortality: https://www.ahajournals.org/doi/10.1161/01.cir.92.9.2396
This is not a new finding. It's common enough to have a name: the cholesterol paradox ( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6374572/ ). Also replicated in a more recent n=100k Denmark study: https://www.bmj.com/content/371/bmj.m4266 These are all observational studies, meaning cause and effect is not established. It's relevant that people with some cancers will have very low cholesterol (the cancer apparentl…
It’s high levels of _oxidized_ LDL that’s problematic. https://youtu.be/DXKJaQeteE0
As a medical field outsider: Instead of basic linear / bell/U curve type ways of describing impact of biomarkers, are new ways of describing complex biomarker relations emerging into the vernacular? e.g. optimums within clusters/sets of biomarkers
This is not a new finding. It's common enough to have a name: the cholesterol paradox ( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6374572/ ). Also replicated in a more recent n=100k Denmark study: https://www.bmj.com/content/371/bmj.m4266 These are all observational studies, meaning cause and effect is not established. It's relevant that people with some cancers will have very low cholesterol (the cancer apparentl…
Alternative hypothesis: high cholesterol is correlated (a small part of TC is from eating) with some adverse medical condition that statins are effective against. From this cohort, statin users measure lower cholesterol and die less. That lower cholesterol is always desirable and we should stop eating eggs would make absolutely no sense.
This is not a new finding. It's common enough to have a name: the cholesterol paradox ( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6374572/ ). Also replicated in a more recent n=100k Denmark study: https://www.bmj.com/content/371/bmj.m4266 These are all observational studies, meaning cause and effect is not established. It's relevant that people with some cancers will have very low cholesterol (the cancer apparentl…
Please enlighten us how you know statin health effects are 100% related to the fact their usage happen to reduce TC measurements, as your entire post assumes that. Alternative hypothesis: high cholesterol is correlated (a small part of TC is from eating) with some adverse medical condition that statins are effective against. From this cohort, statin users measure lower cholesterol and die less. That lower cholesterol…
However, logically my post does not entirely rely on knowing the precise in vivo mechanism of statins and their causal health effects. We only need to see that in RCTs, lowered cholesterol doesn't cause increased mortality as these observational studies would suggest. That is a pretty direct test of the null hypothesis.
edit re your alternative hypothesis: what is this underlying adverse medical condition, and how is it resolved by statins? Every source I can find agrees statins work straightforwardly by inhibiting biosynthesis of cholesterol in the liver.