Longwell3 said:
I am trying to visualize the calcium in the bloodstream. It is ALL in the same form, completely dissolved?
Completely dissolved ≠ all in the same form. The calcium ion can be complexed (bound) by different species in the bloodstream, but under normal conditions none of it will be a solid like you're thinking of.
Longwell3 said:
If you swallow a particle of ground oyster shell it instantly dissolves into these identical ions which are all equally available to the cells?
Thanks. does "dissolved" mean all single, free ions? (one nucleus and and odd number of electrons), no larger aggregates will survive the stomach acid?
Nothing happens instantly. The larger the particle of calcium carbonate, the longer it will take to dissolve. I suppose that if it's big enough, it won't dissolve completely in your stomach, in which case it will move into your intestines and get excreted. It certainly won't enter the bloodstream as a solid.
Longwell3 said:
I , for example, have been disagnosed with "calcific aoritc valve." Trying to understand the actual form of calcium that is aggregating there. How and why.
Standard disclaimer: we can't dispense medical advice on PF.
That said, this article (might be paywalled) has some information:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888946/
Abstract:
Calcification occurs in atherosclerotic vascular lesions and in the aortic valve. Calcific aortic valve disease (CAVD) is a slow, progressive disorder that ranges from mild valve thickening without obstruction of blood flow, termed aortic sclerosis, to severe calcification with impaired leaflet motion, termed aortic stenosis. In the past, this process was thought to be ‘degenerative’ because of time-dependent wear and tear of the leaflets, with passive calcium deposition. The presence of osteoblasts in atherosclerotic vascular lesions and in CAVD implies that calcification is an active, regulated process akin to atherosclerosis, with lipoprotein deposition and chronic inflammation. If calcification is active, via pro-osteogenic pathways, one might expect that development and progression of calcification could be inhibited. The overlap in the clinical factors associated with calcific valve disease and atherosclerosis provides further support for a shared disease mechanism. In our recent research we used an
in vitro porcine valve interstitial cell model to study spontaneous calcification and potential promoters and inhibitors. Using this model, we found that denosumab, a human monoclonal antibody targeting the receptor activator of nuclear factor-κB ligand may, at a working concentration of 50 μg/mL, inhibit induced calcium deposition to basal levels.
I'm not an MD, but it looks like there's some debate as to exactly how the calcium deposits occur. Osteoblasts are bone cells, and they serve to deposit hydroxyapatite (a calcium mineral that makes up a large percentage of our bones), so if they are present, it implies an ongoing (or active) buildup of calcium deposits.