>Using NMR spectroscopy, the researchers found that when the cells become stressed and die, they release PAR, which binds very strongly to calcium ions. Once released, the PAR starts mopping up calcium into larger droplets which stick onto the components in artery walls that give the artery its elasticity, where they form ordered crystals and solidify, hardening the arteries.
But then they don't discuss it at all - just talk about the potential solutions and discovery etc.
Can anyone elaborate on what this means "that when the cells become stressed and die"? Is this something we have control over? Is it related to stress? Does diet & exercise reduce the incidence of this? Is it inevitable?
Or from another angle "Once released, the PAR starts mopping up calcium into larger droplets which stick onto the components" does this imply that reduction of blood calcium (via exercise etc) reduces the impact of these cell deaths?
I don't think you're going to find a straightforward answer because "cells becoming stressed and then dying" is typically a good and normal thing. Cells that refuse the cues to self destruct are roughly synonymous with "cancer cells".
When you undergo vigorous exercise, muscle cells (for instance) that cannot keep up with their energy demands undergo apoptosis and make way for other cells that have more efficient energy production. You can enforce natural selection of efficient mitochondria within your own body with vigorous, stressful exercise.
I encourage you to read the excellent book _Power, Sex, Suicide_ by Nick Lane which covers the topics of energy production in the cells and natural selection of mitochondria, etc. A fascinating book.
I would further encourage you to get as much vigorous exercise as you possibly can. There is no reason to pay any attention at all to trivial dietary and supplement optimizations if you aren't undertaking the intervention that covers the first 99% ...