However, that does not imply that removing coronary calcium will reduce coronary events. In fact, statin therapy by itself actually increases coronary artery calcification.
It turns out that calcified and fibrotic atherosclerotic plaques are not the plaques that rupture and cause thrombosis and myocardial infarction; in fact, the responsible plaques tend to be large, lipid-rich plaques with a thin cap (called thin cap fibroatheromas). Calcium can actually be protective in helping to form robust caps over plaques. There is a lot of work on characterizing cap-Calcium microstructure. Theoretically, removing calcium somehow using drug agents could have an adverse effect.
It is likely true that they tend to form where there are surface defects; this idea is decades old and a component of Virchow's triad.
I would be interested in reading more about this. Do you have any recommendation for a layman?
All the articles are very good.
There a lot of knobs at each step but that's basically it.
>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% ...
Can anyone tell what was patented? I would assume not minocycline, but I've been surprised before about what could be patented.
If they made a brand name minocycline, no one would ever use it because it's already generic. However if they can make a derivative that is more efficacious (even if it's only slightly different), they can brand that and sell it under patent for a while.
Have there been any tests with animals?
How can this ever be allowed?